Furthermore, whereas we have recently reported that KRIT1 loss-of-function results in the sustained upregulation of adaptive redox homeostasis mechanisms that counteract endogenous oxidative stress but sensitize cells to exogenous oxidative and inflammatory challenges [20,26], there is evidence that even established mouse models of atherosclerosis, including ApoE KO [54] and LDL-R KO [55], do not display atherosclerotic plaques within 5 months unless fed a high-cholesterol diet. This evidence concerns the gene LDLR and atherosclerosis.