Fcγ receptors (FcγRs) is an important family of receptors involved in the recognition of IgG- coated particles and complexes. Engagement of activating FcγRs initiates phagocytosis, antibody- dependent cellular cytotoxicity, and the release of inflammatory mediators. Many systemic autoimmune diseases are under FcγR control. Immune thrombocytopenic purpura (ITP) is the most common cause of thrombocytopenia in children. Multiple pathophysiologic mechanisms contribute to thrombocytopenia in ITP, including phagocytosis and destruction of autoantibody-coated platelets. Aim To study the impact of FcγRIIIa polymorphism on development of ITP in Egyptian children, and its impact on bleeding severity, response to treatment and disease chronicity. Subjects and methods: This is a case-control study including 40 patients with ITP (25 newly diagnosed, 15 chronic ITP) and 20 normal controls. Medical history and physical examination were performed. Laboratory investigations included CBC, Coombs test, serum complement and antinuclear antibody, platelet- associated IgG, ELISA test for H. pylori antigen in stools, and FcγRIIIa genotyping by PCR. Patients were followed up for one year to assess severity of the disease and response to treatment. Results: The high affinity FcγRIIIa genotype (158 V/V) and the heterozygous genotype (V/F) were significantly overrepresented in ITP patients compared to the control group. There was no significant difference among ITP patients carrying different FcγRIIIa genotypes regarding response to therapy with corticosteroids or IVIg, and FcγRIIIa genotypes were similar in acute and chronic ITP. Conclusion: FcγRIIIa polymorphism might confer susceptibility to ITP, however, different FcγRIIIa genotypes did not affect response to therapy or development of chronic ITP.