The estimated incidence rate of ITP in adults is 5-10/100,000, and the pathophysiological mechanism is thought that antiplatelet antibodies, such as glycoprotein Ib-alpha (GPIbα) and glycoprotein IIb/IIIa (GPIIb/IIIa), bind directly to platelets, leading to the hyperdestruction of platelets in the spleen and the liver and these antibodies also bind to megakaryocyte, resulting in impaired platelet production [1]. This evidence concerns the gene GP1BA and autoimmune thrombocytopenic purpura.