The Hb S variant decreases the risk of infection by P. falciparum. The mechanism of red blood cells (RBC) resistance in sickle cell trait (AS) individuals could be due to the lack of parasite development and accelerating Hb S polymerization in low O2 tension and higher rates of phagocytosis of parasite-infected sickle erythrocyte by host immune cells [4, 5]. This evidence concerns the gene GSTM1 and infection.