Remarkably, in a small subset of ERα-negative “molecular apocrine” breast cancer [14], AR activates, rather than inhibits, the expression of many ERα target genes through its recruitment to sites that are normally bound by ERα in luminal MCF7 cells [15], suggesting that in ERα-negative breast cancer some NRs can, at least in part, take the role of ERα. This evidence concerns the gene ESR1 and breast carcinoma.