In aged, insulin-resistant, and T2D mice, insulin-secreting pancreatic β-cells became senescent, characterized by upregulation of senescence markers: p21Cip1, p16Ink4a (4), increased activity of SA-βGal, and increased transcription and secretion of the senescence-associated secretory phenotype (SASP) like IL1α and IL6 (4). The gene discussed is INS; the disease is type 2 diabetes mellitus.