Our proteomic approach also pointed to the higher content of proteins participating in platelet adhesion (TSP1, CD36, fermitin family homolog 3, multimerin-1)35,36, activation (GNAI2, TREM-like transcript-1, integrin-linked protein kinase, talin-1, vinculin, filamin A)37–39 and aggregation (GPIIb, GPIIIa) in plasma clots from both APS and VTE patients as compared to healthy controls (Fig. 3). The gene discussed is TREML1; the disease is autoimmune polyendocrinopathy.