Vertex proved the cells. Sana is testing immune invisibility. ProTrans suggests autoimmunity can be reshaped for years.
For most of the last 30 years, Type 1 diabetes “cure research” has suffered from the same structural weakness: too much theory, not enough clinical reality. We’ve had elegant models, promising animal data, and a rotating cast of biotech platforms — but very few human results that forced the field to update its beliefs.
Over the past 12–18 months, that has changed.
Not because Type 1 diabetes is suddenly cured, but because we now have something almost as valuable: a clinically grounded picture of what a functional cure might actually look like. For the first time, the cure conversation is no longer built mostly on hope, extrapolation, and mouse data. It’s being shaped by human evidence — and that evidence is starting to converge on a surprisingly coherent blueprint.
As we’ve previously discussed, identification of Type 1 early leads to the potential for interventions that prolong life without full T1D, however, here we go a step further.
It isn’t a single breakthrough. It’s an engineered architecture: a combination of strategies that each solve a different part of the immune problem that makes Type 1 diabetes uniquely difficult.
And crucially, those components are no longer hypothetical. We now have human evidence for each part of the cure puzzle.
Vertex settled the first argument: the cells can work.
For years, the cure debate started with a basic question: can we make insulin-producing cells that behave like real human islets?
Vertex has now answered that, and the answer is yes.
In 2025, Vertex published one of the most important clinical papers in Type 1 diabetes in decades: “Stem Cell–Derived, Fully Differentiated Islets for Type 1 Diabetes” in The New England Journal of Medicine. It describes early outcomes of zimislecel (formerly VX-880), and it provides clear evidence of glucose-responsive insulin secretion and, in many cases, insulin independence.
You can read the full NEJM paper here:
https://www.nejm.org/doi/full/10.1056/NEJMoa2506549
This matters because it removes the biggest historical uncertainty in the field. The “replacement” side of the cure equation is no longer speculative. The cells can function.
But embedded in that success is the qualifier that now defines the next phase of cure research: the therapy required chronic immunosuppression.
Vertex proved the cells. The immune system still holds the keys.
Type 1 diabetes is not one immune problem. It is two.
If Type 1 diabetes were simply a transplantation challenge, the solution would likely already exist. We know how to prevent rejection. Transplant medicine has decades of experience.
The problem is that Type 1 diabetes isn’t only transplant rejection. It includes a second, disease-specific immune system: autoimmune memory against beta cells.
That distinction is not academic. It’s the reason T1D cure strategies keep breaking late.
Even if transplanted cells were not recognised as foreign tissue, they still resemble the target that the immune system has been trained — for years — to destroy. The immune system is not just reacting to “foreignness.” It is reacting to “beta-cell identity.”
So the cure problem has two immune walls. One is standard rejection. The other is autoimmunity.
And once you accept that framing, the cure stops looking like a mystery and starts looking like an engineering plan: you don’t need one breakthrough. You need two immune solutions.
VX-264 didn’t just fail. It taught the field what won’t be enough.
Vertex’s discontinued VX-264 programme is often treated as an awkward footnote.
It shouldn’t be.
VX-264 tested the simplest “no immunosuppression” concept: take the same proven cells, put them behind a protective device, and let glucose and insulin diffuse while blocking immune attack. In theory, it was the most intuitive next step.
In practice, it didn’t meet efficacy endpoints and Vertex discontinued the programme.
Vertex’s programme update is here:
https://investors.vrtx.com/news-releases/news-release-details/vertex-announces-program-updates-type-1-diabetes-portfolio
If you’re trying to understand the shape of a future cure, VX-264 is highly informative. It suggests that in real humans, a physical barrier alone is unlikely to be enough. The immune system has multiple ways to sabotage transplanted cells even without direct contact. Foreign-body responses, fibrosis, oxygen limitation, inflammatory signalling, and microvascular constraints all become part of the battle.
So VX-264 doesn’t mean “the cure failed.” It means the cure will probably require biological immune solutions, not only mechanical ones.
Sana is testing the next logical step: immune invisibility.
If Vertex proved stem-cell derived islets can work, Sana is attempting to solve the most important remaining question: can we prevent immune destruction without systemic immunosuppression?
Sana’s approach aims to engineer cells so they are less recognisable to the immune system — essentially reducing immune visibility. If successful, this would allow cell replacement therapy to move beyond the narrow subset of people for whom immunosuppression risk is acceptable.
Sana’s six-month clinical update is here:
https://ir.sana.com/news-releases/news-release-details/sana-biotechnology-announces-positive-six-month-clinical-results-type-1-diabetes-study-islet
This is early-stage evidence and should be treated accordingly. But it is still significant because it represents one of the first serious human attempts to demonstrate immune evasion in a Type 1 diabetes cell therapy setting without chronic immunosuppression.
Sana is not yet “the answer.” But it is clearly part of the blueprint.
Because it targets immune wall number one: transplant rejection.
ProTrans adds a different kind of evidence: autoimmunity can be reshaped for years.
NextCell’s ProTrans data sits in a different category.
ProTrans is not a cell replacement therapy. It is a disease-modifying therapy designed to preserve endogenous beta cell function early in Type 1 diabetes through immune modulation.
And that distinction matters, because it speaks directly to immune wall number two: autoimmune memory.
NextCell’s six-year durability update is here:
https://www.nextcellpharma.com/press-releases/six-year-data-demonstrate-a-durable-disease-modifying-effect-of-protrans-in-type-1-diabetes
A report covering the seven-year follow-up is here:
https://theregenreport.com/2026/02/03/nextcell-reports-positive-7-year-data-for-its-stem-cell-candidate-protrans-for-type-1-diabetes/
This isn’t a cure. It doesn’t replace missing beta cells. But it provides something the cure field desperately needs: evidence that immune-modifying cell therapy can have durable, multi-year effects in humans.
And that is precisely what the “combination cure” blueprint requires. Because even if hypoimmune engineering prevents rejection, the autoimmune system may still need to be calmed, re-trained, or suppressed in a targeted way — ideally without the toxicity of broad immunosuppression.
The “Immune-First” What-If: Could modulation come before replacement?
At this point, it’s worth exploring a speculative idea — not as a prediction, but as a logical extension of what the evidence implies.
What if the cure pathway doesn’t start with cell replacement?
What if it starts with immune preparation?
This is not a new concept in immunology. In many diseases, you don’t treat the damaged tissue first — you treat the process that is actively destroying it.
In Type 1 diabetes, the process is immune-mediated beta-cell killing.
So the what-if looks like this: instead of transplanting cells into a hostile immune environment and hoping protection strategies hold, you first attempt to shift the immune baseline — dampening the autoimmune attack, increasing regulatory signalling, and reducing inflammatory tone. Only once the immune system is “less hostile” do you introduce a replacement cell therapy.
In theory, this could make multiple cure strategies easier. Hypoimmune engineering might not need to be perfect. Encapsulation might not need to withstand maximum immune pressure. Even partial protection could become sufficient if the immune system is less aggressive to begin with.
Let’s be even more provocative: could immune modulation be enough for some people?
Now we move further into speculation.
ProTrans and other immune-modulating approaches are typically framed as “disease modifying,” not “curative,” because they don’t replace lost beta cells.
But there is a subtle possibility hiding in that framing.
Many people with long-duration Type 1 diabetes still have tiny traces of beta-cell function. Sometimes it’s so small that it doesn’t meaningfully change insulin dosing — but it can show up as a low but detectable C-peptide.
The question is: what does that tiny residual function represent?
Is it a dying ember that cannot recover? Or is it a suppressed system that could, under the right immune conditions, expand and regain some functional capacity?
There are reasons to be cautious here. Beta-cell regeneration in humans is limited. Long-standing T1D involves structural loss of islets, not just suppression. And immune memory is persistent.
But there is also a reason the idea is interesting: if immune modulation can create multi-year reductions in autoimmune aggression, then in a subset of people — particularly those early in disease, or those with measurable residual function — it is not impossible that the body might stabilise and partially recover insulin secretion.
Not to “normal.” Not to insulin independence. But enough to shift outcomes. Enough to reduce glycaemic volatility. Enough to reduce severe hypoglycaemia risk. Enough to lower long-term complication exposure.
And if the immune system can be moved first, then a future cell replacement therapy might not need to do all the heavy lifting alone.
In that world, immune modulation is not the cure. It is the runway.
The functional cure is starting to look like an engineered combination.
When you connect these evidence streams, the future cure stops looking like a single invention and starts looking like a multi-part design.
Vertex has shown that replacing beta cells at scale is viable. Sana is exploring whether engineered immune evasion can eliminate the need for systemic immunosuppression. ProTrans suggests the autoimmune environment can be modulated for years.
Each one maps onto a different part of the dual immune challenge.
And that’s the core reason this moment feels different from previous “cure hype cycles.” We aren’t just seeing promising science. We are seeing the outlines of a cure architecture supported by human data.
A plausible functional cure by the end of the decade may not be a single therapy. It may be a protocol: immune preparation, cell implantation, and long-term immune stability.
That’s less dramatic than a one-shot miracle.
But it’s how biology tends to be solved.
The Three Milestones That Would Confirm the Blueprint
If this blueprint is real — if Type 1 diabetes is now moving from “hope” to “engineering” — then the next few years should deliver three very specific milestones.
The first milestone is insulin independence without chronic systemic immunosuppression, demonstrated not in a handful of patients for a few months, but in a cohort large enough to rule out luck and durable enough to rule out short-term immune escape. Vertex has already proven insulin independence is possible. The next proof is whether immune evasion strategies can deliver the same outcome without the toxic transplant drug burden. That is the moment cell therapy stops being a niche transplant-like intervention and starts becoming a plausible population-level cure strategy.
The second milestone is evidence that the autoimmune component of Type 1 diabetes can be durably suppressed, reshaped, or functionally neutralised without paying the price of broad immunosuppression. ProTrans is one of the strongest long-duration signals we have so far that immune modulation can last for years. But the question that matters for the cure blueprint is whether immune modulation can be reliably deployed as a platform — something that can prepare the immune system for replacement therapy, or potentially stabilise residual function in those who still have it.
The third milestone is the combination moment: a therapy stack that explicitly treats Type 1 diabetes as a dual-immune problem, not a single obstacle. That might look like immune modulation first, followed by hypoimmune cell replacement. Or it might look like hypoimmune cells delivered into a pre-conditioned immune environment. But the defining feature will be that it is designed, from the outset, to address both immune walls. When we see the first trials built that way — and when they show durable human outcomes — we will know the field has stopped trying to win with a single clever trick and started building the cure as a system.
That is the point where Type 1 diabetes cure research becomes less like a moonshot and more like a roadmap.
Then, of course, there’s the other question associated with the Roadmap. At what cost?
How can these treatments be made affordable, not just effective?
Food for thought
If you want the honest headline for 2026, it’s not “we’ve cured Type 1 diabetes.”
It’s something more important:
We now know what a cure will need to be.
The field has moved beyond speculation. We have proof that stem-cell derived islets can restore insulin production in humans. We have early evidence that immune invisibility is not purely theoretical. And we have long-term signals that immune modulation can last for years.
Type 1 diabetes has two immune walls. That used to feel like the reason cure research would always run into trouble.
Now it looks like a map.
And for the first time in a long time, the cure conversation is starting to look less like hope — and more like engineering.
Only one question remains: Five years or ten?
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