This may be implemented by c-Myc-mediated suppression of the expression of the p21 (Waf1,Cip1), a CDK inhibitor inducible by stabilized p53.[39] It is believed that Per1 overexpression inhibits tumour growth by making damaged cells more susceptible to apoptosis via induction of c-Myc/repression of p21.[59] Dec1 and Dec2 proteins repress Clock/Bmal1-induced transactivation of the Per1 promoter in the mouse via direct interaction with Bmal1 as well as by competing with Bmal1 for the E-box elements in the Per1 promoter.[59]. The gene discussed is BMAL1; the disease is neoplasm.