Per2 mutant mice display a phenotype of accelerated aging (progressive fur graying) after they have received a non-lethal dose of ionizing radiation (an agent producing double-strand breaks), similar to the Atm heterozygous phenotype.[36–38] This was interpreted as signal suggesting that the functions of Per1 and Per2 proteins and Atm converge to a common pathway.[36,38] Later, it was shown that induced expression of Per1 in cancer cells resulted in phosphorylation of Chk2 even in the absence of DNA damage.[39] Per1 overexpression in human cancer cell lines inhibits tumour growth. The gene discussed is PER2; the disease is cancer.