(1) the inhibition the recruitment of TAMs to tumor sites by blocking various chemokines produced by tumor cells and stromal cells [26]; (2) the depletion of TAMs with CSF-1R antibodies [27]; (3) reprogramming TAMs by switching the M2 polarization state to M1 [23]; (4) targeting the immunoinhibitory molecules on TAMs such as leukocyte immunoglobulin-like receptor subfamily B (LILRB) [28] and PD-L1 [29]. Here, CSF1R is linked to neoplasm.