Furthermore, activation of c-ABL1 by the proangiogenic factor, basic fibroblast growth factor (bFGF), promoted endothelial cell proliferation, survival in response to serum-deprivation, motility, tube formation, angiogenesis, and tumor growth of the triple negative MDA-MB-231 breast cancer cells in a xenograft model [33]. This evidence concerns the gene FGF2 and neoplasm.