For example, we found that functional alleles in PLA2G7 do not alter levels of pro-atherogenic lipids (e.g. LDL-cholesterol), suggesting that such pro-atherogenic lipids do not mediate associations between Lp-PLA2 activity and CHD and supporting the need to adjust epidemiological associations of Lp-PLA2 activity with CHD risk for pro-atherogenic lipids (an approach which yields results consistent with non-causality).3 This evidence concerns the gene PLA2G7 and coronary artery disorder.