VEGFA and neoplasm: Several mechanisms of resistance to antiangiogenic treatment have been explored, including tumor infiltration by myeloid cells producing proangiogenic ligands, activation of VEGF-independent angiogenic pathways due to overexpression of alternate mediators, in-situ tissue expression of angiogenesis-related markers (such as VEGF, PDGF-C, delta-like 4 (DLL4) and Neuropilin-1) and polymorphisms in the VEGF signalling [11].