In the context of SLE predisposing loci, Clatworthy et al. [89] have shown that FCGR2B is important in controlling the immune response to Plasmodium falciparum, the parasite responsible for the most severe form of malaria, and suggests that the higher frequency of human FCGR2B polymorphisms predisposing to SLE in Asians and Africans may be maintained because these variants reduce susceptibility to malaria. The gene discussed is FCGR2B; the disease is systemic lupus erythematosus.