In contrast to the positive interactions between PRL and growth factors in these transgenic murine and breast cancer models, PRL and EGF have been reported to oppose one another in “normal” mammary cell lines, such as HC11 and NMuMG; the phenotype of the target cell is likely to be critical in dictating the outcome of PRL signals and crosstalk with other signals (112, 116). The gene discussed is PRL; the disease is breast cancer.