The epistatic gene in these cases was α+-thal, whereby the relative deficiency in α+-thal genes in combination of HbAS or HbSS causes decreased intra-erythrocytic concentration of Hb S. The importance of the Hb S concentration in protection and or susceptibility to malaria has been corroborated by a murine study that reported low P. yoelii parasitemia in transgenic mice engineered to have high Hb S compared to severe infections and death in those with low Hb S [16]. The gene discussed is GSTM1; the disease is malaria.