In recent studies, we have demonstrated in breast cancer ERα+ and HER2+ cells, up-regulation of PRLR transcription/expression induced by endogenous/exogenous PRL in the absence of estrogen via the long form of the prolactin receptor with essential participation of ERα and JAK2/STAT5, mitogen-activated protein kinase (MAPK) and PI3K pathways [5]. The gene discussed is PRL; the disease is breast cancer.