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. This evidence concerns the gene CRY1 and atherosclerosis.