In APS, the development of thrombosis is associated with reduced endothelial NO through the binding of aPL to the apolipoprotein E receptor 2 (ApoER2) by β2GPI, which leads to the protein phosphatase 2A (PP2A) activation that induces eNOS dephosphorylation (Sacharidou et al., 2018). The gene discussed is PTPA; the disease is autoimmune polyendocrinopathy.