Confirming the involvement of VEGF in melanoma development, the anti-VEGF monoclonal antibody (mAb) bevacizumab (FDA-approved for various metastatic cancers) inhibited the proliferation of VEGFR-2+ (but not of VEGFR-2neg) cell lines, but did not cause cell death; survival was at least in part mediated by mTOR pathway, as co-treatment with bevacizumab and rapamycin caused VEGFR-2-dependent loss of half of the VEGFR-2+ cells (106). This evidence concerns the gene VEGFA and metastatic malignant neoplasm.