Sickle cell trait (SCT), which offers protection against malaria, is a point mutation in only one of two beta-globin genes on chromosome 11, as seen in Figure 1, which differentiates it genetically from SCD. SCD (genotype hemoglobin [Hb] SS, HbSC, and other variants) clinically presents with a range of complications, while SCT (genotype HbAS) is mainly considered a benign condition; however, complications such as venous thromboembolism, exercise-related injury, and renal complications have been identified [1]. This evidence concerns the gene GSTM1 and Schnyder corneal dystrophy.