The basis of this clinical benefit may be attributable to the immunomodulatory effects of anti-VEGF/TKI, including enhanced dendritic cell maturation, increased effector T-cell and decreased regulatory T-cell, and myeloid-derived suppressor cell tumor infiltration, which lead to a tumor microenvironment favorable for generating anti-tumor immune responses, which in turn leads to potentiation of IO efficacy [19,20,21,22]. The gene discussed is VEGFA; the disease is neoplasm.