Compositions and methods for inhibiting inflammation of vessel wall and/or formation of neointimal hyperplasia by gene therapy using a soluble Flt-1 (sFlt-1) gene, are provided. VEGF has an essential role in the development of neointimal hyperplasia by causing inflammation. sFlt-1 gene transfer to the site of vascular injury blocks Flt-1-mediated VEGF signal transduction, thereby inhibiting early inflammation as well as late neointimal hyperplasia. The present invention is useful for inhibiting or treating inflammation of vessel wall and/or formation of neointimal hyperplasia in a patient with risk of post coronary intervention restenosis, atherosclerosis, arteriosclerosis, or edema.