Alterations in leukocyte–endothelial interactions were mimicked by using a CLOCK/BMAL1 inhibitor (CLK8), which allowed us to demonstrate that circadian clock alterations in immune cells promote enhanced interaction of these cells with the endothelium, a mechanism that may underlie the high atherosclerotic risk associated with type 2 diabetes. The gene discussed is BMAL1; the disease is type 2 diabetes mellitus.