Current studies emphasize the cGAS–STING axis in DR-linked endothelial senescence but overlook cell-type-specific triggers (e.g., mitochondrial vs. nuclear DNA damage) and fail to address how obesity-linked inflammation in type 2 diabetes may synergistically amplify STING activation, a gap unmodeled by STZ-induced diabetic models. This evidence concerns the gene STING1 and type 2 diabetes mellitus.