Several preclinical and clinical studies have demonstrated that CSF1R inhibitors, including small-molecule tyrosine kinase inhibitors (e.g., PLX3397, GW2580, and Ki20227) and monoclonal antibodies targeting CSF1R or its ligand CSF1, can effectively deplete or reprogram TAMs, thereby improving tumor immune contexture and enhancing the efficacy of ICIs (161). This evidence concerns the gene CSF1R and neoplasm.