Mice with an NHEJ (non-homologous end joining) deficiency undergo rapid lymphomagenesis, and a hypomorphic p53 mutant p53R172P that lacks apoptotic function but retains the ability to induce senescence can rescue lymphomagenesis, but also induces severe diabetes accompanied with the senescence of pancreatic β cells [117]. This evidence concerns the gene TP53 and diabetes mellitus.