CCL5 and pancreatic ductal adenocarcinoma: Moreover, research indicated that SMAD deficiency in pancreatic ductal adenocarcinoma (PDAC) cells activated IFN-I and stimulator of interferon genes (STING) signaling to increase the expression of C-C motif chemokine ligand 5 (CCL5) and C-X-C motif chemokine ligand 10 (CXCL10), thereby enhancing immune recognition and improving the antigenicity of tumor cells96.