In this study, to further asses the pathomechanism of KC after CXL, we evaluated the short and the long-term effect of CXL on the concentration of mediators (IL-6, -13, -17A, IFNγ, CXCL8, CCL5, MMP-9, -13, TIMP-1, tissue plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1), EGF and NGF in tears of patients with KC. This evidence concerns the gene CCL5 and keratoconus.