In SCD liver, the lack of hypoxia-induced nuclear factor-κB p65 activation, along with the imbalance in the endothelial/inducible nitric oxide synthase response to I/R injury and the inability to increase hypoxia-induced expression of HO-1/biliverdin reductase, contribute to liver injury that leads to apoptosis and fibrosis [54]. This evidence concerns the gene NOS2 and Schnyder corneal dystrophy.