demonstrated that while PRL increased oncogenic potential in breast cancer cells by stimulating HOXA1, which in turn induced STAT5, ERK phosphorylation, and increased transcriptional activity of ELK1, SAP1A, STAT5A and B to increase cell proliferation, survival and anchorage dependent growth, following treatment with Δ1-9-G129R-hPRL (65). The gene discussed is PRL; the disease is breast cancer.