First, environmental factors, such as viral or bacterial infection, affect the development of allergic and autoimmune diseases.[16] Second, FcγRIIb, a low-affinity IgG Fc receptor, has been shown to play a role in both allergic disease and ITP.[17,18] In addition, FcγRIIIa genetic polymorphisms play a role in the pathogenesis of ITP and atopic disease.[17,19,20] Third, compared to Th1 bias, Talaat et al[21] found elevated Th2 cytokines (IL-4, IL-10) in patients with ITP. The gene discussed is IL4; the disease is autoimmune thrombocytopenic purpura.