EGFR and neoplasm: In the TME, the antiangiogenic drugs bevacizumab and ramucirumab can bind to human VEGF and block its biological activity (143–145); cetuximab and panitumumab bind to the epidermal growth factor receptor (EGFR), repolarize TAMs from M2-like to M1-like phenotypes, recruit myeloid effector cells such as M1 macrophages and PMN for tumor cell killing by ADCC (147–149), and inhibit angiogenesis and vascular endothelial permeability (162–164), and thus block M2 cell infiltration in the inflammatory environment and impede tumor development (165–167).