With the maturity of genetic engineering technology, a variety of genetic engineering mouse models for the development of key factors and processes of choroidal neovascularization(CNV)have been adapted to meet the needs of different research points in the CNV process. For example, VEGF₁₆₄ RPE65 transgene, Tet/VMD2/VEGF, etc. which are key factors in the process of CNV. ApoE overexpression rats are an important model of spontaneous CNV formation in AMD-like lesions; Ccl2/Cx3cr1-deficient mice associated with changes in retinal pigment epithelial(RPE); choroidal neovascularization and retinal neovascularization can be seen in SOD1^-/-aging, Vldlr^-/-directed mutation, etc; retinal neovascularization secondary to choroidal neovascularization can be found in Cp^-/-Heph^-/Y knockout mice, etc. The main advantages of the CNV genetic engineering mouse model are rapid induction and short time of occurrence; strong correlation with CNV pathophysiology, which can compare various biological components of CNV and facilitate the study of its mechanism; closely relating to human CNV, and providing research methods for human CNV treatment evaluation. However, there are also limitations, such as low induction rate, low percentage and small area of CNV; frenquent occurrence of retinal angiomatous hyperplasia,which interferences CNV research. Researchers might select the appropriate model according to his own needs and modify the corresponding experimental parameters as needed.