The underlying pathophysiology depends on the formation of autoantibodies directed against endogenous PF4-heparin complexes.1,2 This results in the coating of the platelets by IgG, which are subsequently removed by macrophages in the reticuloendothelial system, leading to thrombocytopenia in roughly 85% to 90% of affected patients.3,4 It also leads to the activation of the platelets by an unknown mechanism, which increases the risk of both arterial and venous thrombosis, occurring in roughly 50% of affected individuals. The gene discussed is PF4; the disease is Thrombocytopenia.