The hypercholesterolemia that occurs in the Apoe−/− mice following STZ administration has been considered a shortcoming in this mouse model of human diabetic cardiovascular disease (Renard and Van Obberghen 2006; Hsueh et al. 2007; Kanter et al. 2007; Ramasamy and Goldberg 2010) and, in our case, may mask any macrovascular protective effects that are due to reducing dicarbonyl stress through overexpression of GLO1. This evidence concerns the gene APOE and familial hypercholesterolemia.