The main mechanisms include: redundancy of VEGF signaling (such as up-regulation of VEGFC and PIGF); Changes in biological characteristics of tumor cells (invasion and metastasis, enhanced stem cell characteristics, autophagy and metabolic reprogramming); The pro-angiogenic effects of bone marrow-derived cells (MDSCs, TAMs) and local stromal cells (pericytes, CAFs); And alternative models of angiogenesis (co-selection and mimicry) [17]. The gene discussed is VEGFA; the disease is neoplasm.