We proposed two hypotheses based on the known mechanisms of antiangiogenic drug resistance and the functions of MAGEA3: (1) Although MAGEA3 inhibits VEGF expression, it may activate other alternative angiogenic factors to maintain angiogenesis and provide adequate nutrition; (2) MAGEA3 may alter the metabolic state of tumor cells, enabling them to continue growing under ischemic conditions. Here, MAGEA3 is linked to neoplasm.