The main mechanisms underlying the emergence of acquired resistance to the used anti-angiogenic therapies is the epithelial to mesenchymal transition [53] and the compensation of blocked receptors as well as the activation of alternative proteins or signaling pathways such as the HGF/c-Met pathway, which could drive tumor angiogenesis or growth independently from VEGFRs [64,65,66]. The gene discussed is HGF; the disease is neoplasm.