A reduction in the levels of several individual PC and lyso-PC species has previously been reported in patients with atherosclerosis in comparison to those of healthy subjects via a targeted metabolomics approach [36], indicating that abnormal glycerophospholipid metabolism might be correlated with the aberrant activity of several enzymes, such as PLA1, PLA2 and LCAT, crucial components of oxidized LDL (Ox-LDL), which contributes to atherogenesis [37, 38]. This evidence concerns the gene POU2F3 and atherosclerosis.