The central role of eNOS dysfunction in the onset of atherosclerosis has been further confirmed by in vitro discoveries showing that in ECs, oxLDLs, via LOX-1 activation, elicited a time-dependent decrease in serine 1179 phosphorylation of eNOS, causing its inactivation and, at the same time, the impairment of physiological NO-mediated suppression of iNOS gene expression [41,80]. This evidence concerns the gene OLR1 and atherosclerosis.