Androgen receptor (AR) signaling plays a key role in prostate development, adult prostate function, and prostate cancer. Thus, androgen deprivation therapy remains the mainstay of treatment for prostate cancer, reducing the binding of androgens such as dihydrotestosterone (DHT) to AR to prevent nuclear translocation and subsequent transcriptional activity of AR. However, many prostate cancers that initially respond to androgen deprivation therapies ultimately become castration-resistant, leading to recurrence. The goal of our lab is to study the functions of androgens in progenitor cells, and investigate mechanisms for intrinsic castration resistance from the perspective of developmental and stem cell biology.