Since the aforementioned data indicate that abnormal TNF-α release may represent a potential new target to prevent bone resorption following a joint bleed in mice, we aimed at determining whether systemic levels of TNF-α and synovial tissue expression of this proinflammatory cytokine and its receptors could be increased and related to the development of proliferative synovitis in hemophilia A patients with severe HA. The gene discussed is TNF; the disease is hemophilia A.