FkB2 and REL were found exclusively in stromal cells, and maintained this distribution after castration. In contrast, the expression of RelB in the stroma was suppressed in response to androgen deprivation. Figure S1 summarizes these findings. By comparing the gene expression profiles in the prostate under different hormonal conditions, we identified seven TF, which were further characterized with respect to their expression in the prostate and possible variations in response to castration. These TF were found to be differentially expressed and were grouped in three functionally important groups: coordinators of the immaturity state or regulators of epithelial differentiation, coordinators of the ability of the organ to function as an immune barrier, or early-response genes or genes related to the response to extracellular signaling, which together coordinate the epithelial and/ or stromal cell behavior under androgen-deprived conditions. It is well understood that treatment with androgens increases the AR and coactivator occupancy in the PSA enhancer and promoter regions. Although the regulation of genes such as PSA by the AR in prostate cells seems to be relatively simple, and the prostate weight loss after castration is a direct effect, complex mechanisms are involved in the adaptation of the gland to varying levels of androgen stimulation. We considered that extracting information from the mass of genes revealed by the present experiments using the usual tools could be misleading, in the sense that some regulatory molecules might show subtle or no variations in mRNA content and might escape detection in assays of differential expression. Therefore, we defined an experimental approach to filter for druggable TF that could function as state-defining regulatory hubs by orchestrating different functions related to tissue remodeling and as regulators of differentiation, among others, and localizing these TF to either the epithelium and/or the stroma, and employed a MST to determine the correlation among their expression levels is a number of tissues. We identified TF genes in regulatory networks established from the enrichment terms and from the analysis of the proximal promoter region of the genes that were regulated by androgen deprivation, as revealed by the microarray analysis and referenced not only to the normal androgen levels in non-castrated rats, but also to the high-dose estrogen stimulus. The search for biological relationship between the TF found in the selected networks and the steroid hormone receptors Ar, Esr1 and Esr2 was unveiled by calculating their expression correlation and constructing a MST. MYBL2 is related to proliferative activity. Use of the MMTVPyMT mouse was instrumental in the discovery that Myb is essential for the development of mammary tumors, but not ultimately for their progression.