Moreover, in the APS group compared to VTE patients or healthy controls, we observed within the clots increased amounts of proteins involved in platelet activation and aggregation, such as platelet glycoprotein 4 (CD36), adenylate cyclase-inhibiting G alpha protein (GNAI2), and thromboxane-A synthase (TXS) (Fig. 2D, Supplemental Table 1). The gene discussed is CD36; the disease is autoimmune polyendocrinopathy.