The surviving β cells in T1D islets showed impaired electrophysiological activity, transcriptional signatures of increased antigen presentation (increased MHC class I– and IFN-γ–related pathways, both key in T1D pathogenesis), a shift towards glycolysis, downregulation of mitochondrial respiration, and impaired protein translation relative to β cells from nondiabetic islets changes suggesting metabolic reprogramming of these immune-stressed cells. The gene discussed is IFNG; the disease is type 1 diabetes mellitus.