However, most genetic variants have a stronger impact on severe compared with mild malaria or parasitemia.65 Finally, antibody responses to antigens expressed on the surface of infected red blood cells66 or sporozoites, as well as T cell responses, Fc-receptor polymorphisms,67–69 and donor-specific differences in effector cell phenotypes and FcγR expression13,70 may have confounded our analyses and need further study. Here, FCGR2A is linked to parasitic infectious disease.