Androgen and estrogen receptors are steroid hormone-induced nuclear transcription factors that interact directly or indirectly with chromatin to regulate transcriptional programs within cells during phases of normal growth and differentiation or as part of pathogenic processes, particularly of reproductive endocrine tumours. The androgen receptor (AR) is a key oncogenic driver and therapeutic target in prostate cancer and new generation anti-androgen therapies are available that potently inhibit AR signalling. These AR target therapies are now being actively employed in breast cancer, with clinical trials underway to examine their efficacy in the treatment of metastatic disease. As the large majority of primary and secondary breast cancers express the AR, it represents a prevalent therapeutic target. However, unlike prostate tissue, AR signalling appears to have dichotomous, context-dependent roles in breast cancer. In normal breast tissue, AR signalling exerts an anti-estrogenic, growth inhibitory influence that appears to be sustained in most estrogen receptor (ERα) positive breast cancers. In this context, novel selective AR modulators (SARMS) are being investigated as breast cancer therapeutics. Conversely, evidence has been accumulating to support the concept that AR exerts an oncogenic influence in ERα negative breast cancer and AR antagonists and androgen biosynthesis inhibitors are currently in clinical trials. Understanding the molecular mechanisms whereby AR interacts with chromatin to regulate distinct gene expression programs in different breast cancer contexts is critical to the effective deployment of new AR targeting therapies for treatment of women with breast cancer. Our goal is to develop robust markers of AR action to facilitate patient selection for currently available AR target therapies and characterize novel agents or selective AR modulators as a new wave of breast cancer therapeutics.