Prolactin (PRL) signaling is upregulated in hormone-responsive cancers. The PRL receptor (PRLR) is class I cytokine receptor that signals via the JAK–STAT and MAPK pathways to regulate cell proliferation, migration, stem-cell features, and apoptosis. Patients with pancreatic ductal adenocarcinoma (PDAC) have high plasma levels of PRL. We investigated whether PRLR signaling contributes to growth of pancreatic tumors in mice.