Compared to controls, the patient epithelium overexpressed gelsolin (GSN), alpha enolase (ENOA), S100A4 and cytokeratin3 (KRT3), which suggests a plausible role of these proteins in the pathogenesis of keratoconus [60] while possibly associating the role of structural proteins and enzymes in keratoconus. This evidence concerns the gene KRT3 and keratoconus.