Mutation of the Clock gene accelerates atherosclerosis in Apoe−/− and Ldlr−/− mice,45 while overexpression of the Cry1 gene protects Apoe−/− mice from atherosclerosis development.46 These mouse models show significant alterations in cholesterol metabolism and inflammatory state, both likely contributing to the observed phenotype. The gene discussed is CLOCK; the disease is atherosclerosis.