Collectively, our findings revealed that in ER+ and ER- breast cancer cells, AR activation induces an interaction with GATA3 that results in creation of AR-dependent GATA3 chromatin binding events that are predominantly associated with AR target genes, where GATA3 acts as an AR co-factor to regulate a gene program that promotes a luminal epithelial phenotype and can facilitate its role as a tumor suppressor. Here, GATA3 is linked to neoplasm.