Based on a strong expression of cathepsins B and L in distinct subsets of TAM, which we detected during carcinogenesis in both mouse models of pancreatic cancer and isolated pancreatic tissue of patients, we investigated whether pharmacological cathepsin inhibition leads to disruption or alteration in intracellular signaling pathways that are necessary for the preservation of the M2 phenotype. The gene discussed is CTSB; the disease is pancreatic neoplasm.