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). This evidence concerns the gene VCL and autoimmune polyendocrinopathy.