VEGFA and neoplasm: Recently, we reviewed the following several mechanisms of AAT resistance in tumors [6,7]: (1) hypoxia due to tumor vascular pruning and increase in subsequent angiogenic factors such as VEGF, (2) microenvironments related to different phenotypic characteristics of ECs in tumor and in normal tissues and the evolution of endothelial heterogeneity, (3) extracellular vesicles (EVs)-mediated crosstalk between tumor cells and ECs, (4) inability of VEGF to be effectively recognized by therapeutic agents because of packaging and masking of VEGF by EVs, and (5) stromal stiffness of the tumor.