ITP triggered by the infection of H. pylori has been proved by plenty of mechanisms put forward, including molecular mimicry resulted from the generation of autoantibodies against CagA and the cross-reactivity of the antibodies with platelet surface antigens, phagocytic perturbation by enhanced phagocytic activity of monocytes, platelets aggregation on account of the existence of anti-H. This evidence concerns the gene S100A8 and autoimmune thrombocytopenic purpura.