Interestingly, the NO deficiency, as well as the increased arginase activity and ROS production, evoked by hypercholesterolemia or Ox-LDL are not observed in endothelial cells absent of LOX-1, suggesting the critical role of LOX-1 in mediating arginase-dependent NO deficiency and oxidative stress (117). This evidence concerns the gene OLR1 and familial hypercholesterolemia.