Some β-cells in T2D donors have comparable INS expression levels with those in healthy donors; β-cells in T2D have normal INS expression under low cellular stress, but they have dysfunction under high cellular stress; β-cells in healthy people can deal with the cellular stress, maintaining normal INS expression; oxidative stress could be a major influential factor on INS expression; TNFR1-, BAX-, CAPN1- and CAPN2-dependent pathways may be curial for β-cell apoptosis in T2D; INS and death executioner caspases are differentially expressed among donors. This evidence concerns the gene INS and type 2 diabetes mellitus.