As detailed in the first part of this review, in the last years a number of studies have identified several genes involved in thrombosis, inflammation and endothelial dysfunction altered in APS patients (i.e., TF, PAR1, PAR2, VEGF, Flt1, IL8, TLR2, TLR4, etc.), most of them showing increased expression in cells integrating the immune and vascular systems, including monocytes, platelets, neutrophils and endothelial cells, favoring the thrombin generation, and leading to a procoagulant activity (17, 20, 23, 25–27). This evidence concerns the gene TLR2 and autoimmune polyendocrinopathy.