Under hypoxia sickle Hb (Hb S) polymerizes into long, rigid, and insoluble fibers causing the primary pathophysiology associated with SCD, which leads to RBC sickling, vaso-occlusion, painful crises, organ damage, oxidative stress, hemolysis of RBCs, decreased vascular NO bioavailability, inflammation, impaired microvascular blood flow, morbidity and even mortality [3,4,5,6]. Here, GSTM1 is linked to Schnyder corneal dystrophy.