Other mechanisms that may further contribute to increased oxidative stress in SCD include high mobility group box 1 (HMGB1)-mediated TLR4 signaling, that activates the NF-κB pathway and may affect endothelial CAMs’ expression (e.g., P-selectin), and mitochondrial dysfunction in platelets, in addition to non-heme-dependent mechanisms [114,121,122]. The gene discussed is SELP; the disease is Schnyder corneal dystrophy.