We speculated that, if a cross-talk between HER2 and autocrine prolactin/PRLR signaling is actively involved in the well-known FASN overexpressing-phenotype of HER2-positive breast cancer cells [36, 95–98], blockade of PRLR should then reduce the ability of HER2 to constitutively up-regulate FASN gene expression. The gene discussed is ERBB2; the disease is breast cancer.