Ramucirumab and other anti-VEGF-VEGFR2 agents may modulate the tumor microenvironment to be more immunosupportive or inflammatory, and increase the efficacy of checkpoint inhibitors via several possible mechanisms, including increasing the trafficking and infiltration of CD8+ T cells into the tumor, increasing the expression of major histocompatibility complex-1 and PD-L1, and reducing the frequency of immunosuppressive regulatory T cells markers [23,24,25]. This evidence concerns the gene KDR and neoplasm.