A previous study showed that targeted deletion of Group V secretory phospholipase A2 could significantly alter atherosclerotic lesion area in LDLR−/− mice but not apoE−/− mice, which was attributed to different composition and oxidative status of LDL between such strains [52], and might also lead to the discrepancy of atherosclerosis burden observed in our study. This evidence concerns the gene LDLR and atherosclerosis.