Uveitis is a group of inflammation diseases involving the iris, ciliary body, choroid, vitreous body, retina and retinal vessels, which can lead to visual deterioration and even visual loss. The pathogenesis of uveitis is complex and diverse, including infection, autoimmunity, trauma, physical and chemical injury, immune genetic mechanism and so on. Recent studies have shown that the activation of complement system is one of the pathogenesis of uveitis. Various complement proteins, including CFH, CFB, CFI, MAC, CD59 and so on, regulate host tissue damage through a rigorous mechanism mediated by the complement system. And studies have found that those complement proteins are involved in the occurrence and development of uveitis at the gene level and biological function. In addition, complement components like C2, C3, C4 and C5 can affect the pathogenesis of uveitis in terms of copy number variation, gene polymorphism and the regulation of T-cell-mediated autoimmune response. Therefore, complement inhibition therapy and related gene therapy provide new ideas and targets for the treatment of uveitis.