We show that a defective CD209 response (mediated by G mutant allele) presented with significantly higher parasitemia and anemia (indicated by a low PCV) compared to the wild type variant, demonstrating its role in driving immune responses to malaria, more so than STAT6 (rs3024974) or CD28 (rs35593994) polymorphisms. The gene discussed is CD28; the disease is parasitic infectious disease.