Immune thrombocytopenia (ITP) is an autoimmune disease primarily characterized by increased clearance of auto-antibody-sensitized platelets by Fc-receptor-bearing macrophages in the spleen and liver. It has been classically accepted that antibody-mediated platelet destruction is Fc dependent. Recent studies, however, may also indicate the involvement of Fc-independent pathways of platelet destruction. Current treatment options work by immunosuppression (e.g., corticosteroids), immunomodulation (e.g., IVIg and anti-D), or removal of the platelet destruction site (splenectomy) in ITP. This review will discuss the mechanisms of action of these and other treatments for ITP.