On the other hand, it is the crosstalk regulation and compensatory inhibition between pathways: preclinical studies have shown that the use of anti‐VEGFR drugs alone can upregulate MEK–ERK signaling through a compensatory mechanism (such as activating the RTK bypass pathway) to maintain tumor survival [15], while the use of anti‐MEK drugs alone may increase VEGF secretion by feedback activation of hypoxia‐inducible factor (HIF‐1α) to promote angiogenesis [16]. The gene discussed is KDR; the disease is neoplasm.