Consistent with these data, it was demonstrated in the UK Biobank that apolipoprotein B100 also does not explain the ASCVD risk mediated by Lp(a), but that it does explain the risk mediated by LDL-C.27 This further implies that other components of Lp(a), such as its content of oxidized phospholipids,28 antifibrinolytic effects,29 or potential pro-platelet effects,30 may be more important in mediating clinical manifestations. Here, LPA is linked to atherosclerosis.