The inhibition of colony-stimulating factor 1 receptor (CSF1R), which is ubiquitously expressed by TAMs and MDSCs, have been shown to improve the efficacy of anti-PD1 or anti-CTLA4-based immunotherapy in pancreatic cancers by depleting TAMs and reprogramming the activity of the remaining macrophages [94]. This evidence concerns the gene CSF1R and pancreatic neoplasm.