Endoplasmic reticulum (ER) stress signaling through activation of GSK3β is involved in a mechanism of accelerated atherosclerosis in hyperglycemic, hyperhomocysteinemic, and high-fat-fed apolipoprotein E-deficient (apoE(−/−)) mouse models; McAlpine et al. showed that atherosclerosis can be attenuated by promoting GSK3β phosphorylation [79]. This evidence concerns the gene GSK3B and atherosclerosis.