A study aimed at determining the roles of E2F1 and SRSF2 in VEGF-A expression and pre-mRNA splicing found that SRSF2 overexpression increased the production of the VEGF165b splice variant, an inhibitor of the growth of several types of tumors, by inhibiting the migration and proliferation of endothelial cells 67, resulting in a decrease in tumor neovascularization and tumor formation 68. This evidence concerns the gene SRSF2 and neoplasm.