TRIB3 impairs IRS-1/Akt signalling in endothelial cells mediated by insulin [47], leading to reduced endothelial nitric oxide synthase (eNOS) and NO bioavailability [46], which is associated with endothelial dysfunction and increased leukocyte adhesion to endothelial cells, important steps for atherosclerotic lesion formation (Figure 1) [9]. The gene discussed is INS; the disease is endothelial dysfunction.