In order to shed light on the role of PRL and PRLR in the pathogenesis of GBM, we evaluated proliferation, viability, chemosensitivity and migration of GBM cells in response to PRL stimulation or PRLR signalling blockade using the receptor-specific antagonist ∆1–9-G129R-hPRL (PRLR-A)17, and to the overexpression of the long and short isoforms of PRLR. The gene discussed is PRL; the disease is glioblastoma.