In preclinical tumor models, CSF1R blockade has been shown to effectively reduce TAM numbers, reprogram TAMs toward a more inflammatory M1-like phenotype, and enhance T cell infiltration and function in glioblastoma, pancreatic ductal adenocarcinoma, breast cancer, lung cancer, melanoma, colon cancer, hepatocellular carcinoma, prostate cancer and sarcoma etc (9, 59–63). This evidence concerns the gene CSF1R and neoplasm.