The proposed mechanisms of infection in patients with hemoglobinopathy are interference of phagocytic activities of macrophages and neutrophils from iron overload, lower interferon gamma (IFN-γ) production in Thalassemia patients, and intrinsic virulence of P. insidiosum by carrying a gene encoding ferrochelatase [15,16,17]. The gene discussed is IFNG; the disease is thalassemia.