Clatworthy et al. showed that FcγRIIb-deficient mice had increased clearance of plasmodia-causing malaria, finding that the inhibitory IgG receptor FcγRIIb is important in controlling the immune response to malarial parasites and suggesting that the higher frequency of human FcγRIIb gene polymorphisms might predispose to SLE in Asians and Africans, as these variants reduce patients’ susceptibility to malaria [57]. This evidence concerns the gene FCGR2B and systemic lupus erythematosus.