In order to address this issue, we took advantage of a nonsynonymous TRIB3 Q84R polymorphism (rs2295490), a gain-of-function amino acid substitution impairing insulin signalling, and action in primary human umbilical vein endothelial cells (HUVECs) naturally carrying the TRIB3 Q84 or R84 variant [30, 31], which has been associated with insulin resistance, and early vascular atherosclerosis [31, 32]. This evidence concerns the gene INS and Insulin resistance.