In antiphospholipid syndrome, β2GPI bound Axna2 as high affinity sites on endothelial cells to crosslink with aPL/anti-β2GPI antibodies, triggering the intracellular signaling pathway and inducing inflammation or thrombosis [20,21].Yung S et al. found that the anti-dsDNA antibody bond to mesangial cells depends on Axna2 entering the cytoplasm and nucleus, activating the P38-mitogen-activated protein kinase (MAPK), c-Jun amino-terminal kinase (JNK), and AKT pathways, which induced IL-6 secretion and Axna2 synthesis in a destructive cycle, promoting the development of lupus nephritis [13]. This evidence concerns the gene APOH and antiphospholipid syndrome.