mmune thrombocytopenic purpura (ITP) is a disorder in which antiplatelet antibodies cause accelerated destruction of platelets, resulting in thrombocytopenia and a varying propensity for bleeding. In addition, it is now recognized that these antibodies may also impair platelet production, creating a dual cause of thrombocytopenia. Despite their central role in the immunopathology of ITP, measurement of antiplatelet antibodies remains unreliable, and the diagnosis is made by demonstrating isolated thrombocytopenia without an obvious cause. In most children and some adults, ITP is an acute, self-limited disease that resolves or improves spontaneously within months. In a small number of children and in many adults, ITP may be chronic and poorly responsive to treatment. Most thrombocytopenic patients experience only minor bleeding symptoms, such as epistaxis, petechiae, and bruising. Severe bleeding events, such as intracranial hemorrhage, protracted epistaxis, hematuria, hemoptysis, and gastrointestinal bleeding, are fortunately rare, although their prevention remains the main goal of management. Traditional treatment approaches have focused on inhibiting phagocyte-mediated destruction of antibody-coated platelets. Improved understanding of the disease pathogenesis has initiated development of several new treatments, and the repertoire of therapeutic options for ITP is thereby expanding dramatically. This expansion includes design of more specific inhibitors of platelet destruction that target Fcc receptors (FccRs), such as anti-FccR monoclonal antibodies and molecules that impede FccR-mediated signaling, and thrombopoietic agents that enhance platelet production [1,2].