Multiple mechanisms are linked to the pathogenesis of atherosclerosis, including endothelial dysfunction, which is characterized by an imbalance between endothelium‐dependent vasorelaxation and vasoconstriction,52 the migration and proliferation of vascular smooth muscle cells.53, 54 Breton‐Romero et al17 observed that in aortic endothelial cells derived from patients with T2DM, WNT5A induced impairment of endothelial nitric oxide synthase activation and nitric oxide production was reversed by WNT5A and JNK inhibition (Box5 and SP600125). Here, MAPK8 is linked to endothelial dysfunction.