ABSTRACT Disulfidptosis is a newly identified form of regulated cell death. It occurs under glucose‐starvation conditions and is characterized by metabolic dysregulation in cells with high expression of SLC7A11. Increased cystine uptake under these conditions leads to depletion of NADPH, ultimately triggering cell death. Current research on disulfidptosis has mainly focused on malignant tumors. However, the critical factors involved in disulfidptosis, including high SLC7A11 expression and NADPH depletion, may have potential relevance to type 2 diabetes mellitus (T2DM). Both insulin secretion and insulin resistance are regulated by NADPH levels, and SLC7A11 also plays a key role in glucose metabolism through maintaining redox homeostasis. Although the direct connection between disulfidptosis and T2DM remains to be experimentally verified, this review integrates existing studies to systematically examine their theoretical relationship from both mechanistic and therapeutic perspectives. It focuses on the roles of SLC7A11, NADPH, and other related factors in T2DM and its complications, aiming to provide a theoretical basis for developing new treatment strategies for diabetes.