However, blocking of tumor-associated macrophages (TAM) infiltration into tumors by inhibiting CSF1R signaling has a limited level of success, which is very likely explained by a mechanism that CSF1R inhibition unleashed the expression of granulocyte-specific chemokine in carcinoma associated fibroblasts, thus resulting in infiltration with tumor-associated neutrophils (TAN) (89), also referred to as polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC). This evidence concerns the gene CSF1R and neoplasm.