Deregulation of the expression of c-Myc is believed to constitute a major pathogenetic mechanism in the establishment of the cancer-prone phenotype of Per2-mutant mice, and a risk factor for tumour growth in wildtype mice with disrupted circadian cycle.[38,58] As the mechanisms of induction of DNA repair and apoptosis are, however, partially redundant, elevated levels of c-Myc may route the damaged cells directly to apoptosis, without induction of cell cycle arrest for attempted repair. The gene discussed is MYC; the disease is cancer.