Beyond its role in precipitating diabetic nephropathy, IL17 signaling was atherogenic, which was supported by smaller lesion formation in both antiIL17 adenovirus-transfected ApoE-KO mice [147] and IL17 deficient LdlR (low-density lipoprotein receptor)-KO mice under Western diet treatment [148]. This evidence concerns the gene LDLR and diabetic kidney disease.