In contrast, in T1D donor pancreas tissue and in a human islet model of DNA damage-induced senescence, CDKN1A and p21Cip1 upregulation occurs without any increase in CDKN2A or p16Ink4a (1, 34, 35), suggesting that the response of p21Cip1 and p16Ink4a in β-cells depends on the stressor. The gene discussed is CDKN1A; the disease is type 1 diabetes mellitus.