THZ1 treatment could provide an additional avenue singly or in combination with other inhibitory approaches targeting receptor function (PRLR [26], ERα [13]), HER2 [27], ERBB1 [19]) and/or signaling pathways (MAPK, PI3K, c-SRC [13, 19], ERBB1Tyrosine kinase, [19]) to effectively ablate transcription of PRLR and its contribution to breast cancer. This evidence concerns the gene ERBB2 and breast carcinoma.