In addition, autophagic defects in mouse models of pancreatic cancer trigger the expression of pro-inflammatory cytokines such as Chemokine (C-C motif) ligand 5 (CCL5) and IL-6, and increase the infiltration of PMNs and T-cells, which fuel dysplastic transformation and tumor initiation [157]. This evidence concerns the gene CCL5 and familial pancreatic carcinoma.