Interestingly, among the 52 patients with at least LDLR null mutation, we found that patients who developed ASCVD (n = 25) were more likely to have two LDLR null mutations (Additional file 2: Table S9) and presented higher sera concentrations of FA species, LPC species, CAR species, and arachidonic acid-derived oxylipins than those without ASCVD events (n = 27). This evidence concerns the gene LDLR and atherosclerosis.