SOD1 and keratoconus: The increased levels of oxidative stress markers and the decreased antioxidant capacity and antioxidant defenses in KTCN corneas might be involved in the development of this disease.[5] A genomic deletion within intron 2 close to the 5’ splice junction of the SOD1 gene was identified in three patients with KTCN.[20] However, studies conducted in other populations, including Slovenian,[21] Iranian[22] and Ecuadorian,[23] have not confirmed the correlation of SOD1 sequence variants with keratoconus phenotype.