GSTM1 and Schnyder corneal dystrophy: Higher oxidized forms of hemoglobin (HbS, βV6E, and HbE βE26K) from SCD patients cause endothelial dysfunction via a loss of respiratory chain complex activities in isolated endothelial mitochondria, while prolonged incubation with ferryl Hb (HbFe4+) induced bioenergetic reprogramming, including a higher degree of uncoupled respiration and glycolytic rate [54].