In the coming decades, and I predict as soon as 2038, scientists will successfully deploy gene editing and gene-cell therapies to essentially cure or functionally reverse many forms of diabetes. Although diabetes is one of the more complicated diseases to cure, I think the urgent need for a solution will move it up the list as we strive toward a disease-free world.

Analysis: With gene-editing therapies like the treatment for sickle cell already approved by the FDA, the door is open. Casgevy became the first FDA-approved therapy using CRISPR/Cas9 genome editing in 2023. The rapid development of COVID-19 vaccines using genetic medicine technology in 2020 showed the power of this broader revolution. To be clear, those vaccines did not edit genes, but they did prove something important: genetic medicine can move fast, scale globally, and save lives.

That matters. Once a technology works, humanity tends to push it forward. Given the enormous human and financial cost of diabetes, it will almost certainly become a major target. That is why this timeline is aggressive, but not fantasy. A decade may be early. Two decades feels realistic.

My late wife Lisa’s disease, ALSP, brings this home for me personally. Her condition was tied to a single CSF1R gene variant, a cruel reminder that one tiny genetic change can ripple through an entire life and family. The good news is that targeting single genes with CRISPR technology is clearer, and scientists are already pursuing these diseases. That is why single-gene diseases are such an important first target for gene editing. They are not easy, especially when the brain is involved, but they are more direct. One broken instruction. One possible correction. If science can learn to safely repair or work around diseases like ALSP, it builds the path toward harder conditions like diabetes, where many genes, immune pathways, and environmental factors all interact.

For type 2 diabetes, researchers have identified genetic targets and clues such as GCK and HNF1A, which play critical roles in monogenic forms of diabetes, including MODY. Other genes, such as SLC30A8, are linked to glucose regulation and insulin secretion, while TCF7L2 and PPARG are tied to insulin sensitivity, beta-cell function, and broader risk pathways. This is not a simple one-gene fix. It is more like learning the control panel of metabolism. Over time, this research may help treat existing diabetes and perhaps even engineer resistance in high-risk populations.

For type 1 diabetes, the likely breakthrough is not simply editing one diabetes gene. Type 1 is an autoimmune attack on insulin-producing beta cells. So the more realistic path is gene-edited cell therapy: create or transplant insulin-producing cells that can survive, function, and evade immune attack. Pair that with immune therapies, early genetic risk screening, and better prevention, and the future starts to look very different. Not one magic switch, but a system-level repair.

The big picture is clear: single-gene diseases are first because they are clearer. Diabetes comes later because it is messier. But messy does not mean impossible. It means the road is longer, the tools must mature, and the cure may arrive not as one miracle, but as a stack of breakthroughs that finally tip the system back toward health.