Long-lasting inhibition of CSF1R by FF-10101 can continuously prevent the recruitment and polarization of immunosuppressive TAMs in the TME; however, compensatory induction of M-CSF and the recruitment of other immunosuppressive cells, such as PMN-MDSCs and cancer-associated fibroblasts (CAFs), reportedly occur in a secondary resistance mechanism after CSF1R inhibition (39, 40). This evidence concerns the gene CSF1R and cancer.