It has been proposed [48] that the increased phagocytosis of the HbS and HbC infected erythrocytes in the spleen may also result in improved antigen presentation, which could explain an increase of the protective effect against infection with age, as well as the higher immune response to variant surface antigens observed in individuals carrying those hemoglobinopathies [13, 49, 50]. The gene discussed is KRT88P; the disease is hemoglobinopathy.