Growing evidence supports the role of inflammatory stimuli as “second hit” factors in APS-related thrombogenesis, with multiple mediators giving a possible contribution: indeed, increased levels of endothelium-derived microparticles, platelet-leucocyte aggregates, tissue factor-expressing monocytes, complement split products as well as neutrophil products have been described in patients with APS [33],[36], [37], [38], [39], [47], [46], [45], [44], [43], [42], [41], [40]]. The gene discussed is F3; the disease is autoimmune polyendocrinopathy.