APOH and atherosclerosis: Moreover, the OxLDL/β2GPI/anti-2GPI complex induces the differentiation of macrophages in foam cells, which promotes the development of atherosclerosis, possibly through the mechanism by which HNE oxidizes the β2GPI antigen, which it enhances immunogenicity in response to increased anti-β2GPI antibodies and the aPL antibody cross-reacts with OxLDL, facilitating its entry into macrophages and promoting the progression of atherosclerosis [106].