FADS2 and atherosclerosis: Beyond this study, we pursued potential epistatic functions of the inactivated fads2 locus and the PUFA deficiency in the development of atherosclerotic lesions in the apoe−/− and ldlr−/− mutants, two model systems frequently used in the study of the multifactorial molecular pathogenesis of atherosclerosis, which is characterized by dysregulated cholesterol and lipoprotein metabolisms and completely different from our system.