A normalization of lysyl oxidase abundance [199], increased proteoglycan expression (e.g., lumican, mimecan, and decorin) [200], and a reduction in lactate levels in KC-derived corneal fibroblasts following CXL have been reported [200] suggesting that riboflavin/UV-A CXL may modulate ECM deposition and collagen crosslinking at the cellular level in addition to the direct structural modifications to collagen. The gene discussed is LOX; the disease is keratoconus.