Sickle cell anaemia is an autosomal hereditary disorder in which the erythrocytes become sickle shaped. The disorder or disease is caused by the formation of an abnormal haemoglobin called haemoglobin-S. As found out by Ingram (1958), haemoglobin-S differs from normal haemoglobin-A in only one amino acid - 6‌th ‌ amino acid of β -chain, glutamic acid, is replaced by valine. This is the major effect of the allele. During conditions of oxygen deficiency 6 -valine forms hydrophobic bonds with complementary sites of other globin molecules. It distorts their configuration. As a result, erythrocytes having haemoglobin-S become sickle-shaped. Carriers of the sickle cell anaemia gene are protected against malaria because of their particular haemoglobin mutation; this explains why sickle cell anaemia is particularly common among people of African origin. The malarial parasite has a complex life cycle and spends part of it in red blood cells and feeds on haemoglobin. Both sickle-cell anaemia and thalassemia are more common in malaria areas, because these mutations convey some protection against the parasite. In a carrier, the presence of the malaria parasite causes the red blood cell to rupture, making the Plasmodium unable to reproduce. Further, the polymerisation of Hb affects the ability of the parasite to digest Hb in the first place. Therefore, in areas where malaria is a problem, people's chances of survival actually increase if they carry sickle cell anaemia. Thus, sickle-cell anaemia is a potential saviour from malaria.