Although no association was found between TLR2 and TLR4 expression in neutrophils and monocytes and the severity of KC, the fact that the expression of TLRs is strongly associated with systemic levels of proinflammatory molecules indicates that innate immunity may be involved in the pathophysiology of KC since increased levels of IL-6, TNF-α and MMP-9 in tears were associated with the degree of KC evolution. The gene discussed is TLR2; the disease is keratoconus.