Multi-target agents such as TKIs and aflibercept (anti-VEGF-A and -B) produced better clinical results in the regulation of tumor angiogenesis than the single-target agent bevacizumab (anti-VEGF-A) because tumors readily overcame the inhibition of angiogenesis by activating compensatory pathways such as PDGF or FGF signaling, or both [2,5]. Here, VEGFA is linked to neoplasm.