Moreover, using KRIT1 haploinsufficient (KRIT1+/−) mice, we addressed the hypothesis that heterozygous KRIT1 deficiency may predispose to a greater susceptibility to develop aortic fatty streaks—an early stage of atherosclerosis—under stressful conditions, including pro-oxidant and pro-inflammatory conditions induced by a chronic consumption of high fructose diets [39]. This evidence concerns the gene KRIT1 and atherosclerosis.