However, given that androgen receptor (AR) function is indispensable for male bone formation and remodeling51,52, and that androgens regulate PKC-δ transcription and modulate its apoptotic function in prostate cancer cells53, and prenatal testosterone exposure induces hypertension in adult females via an AR-dependent PKC-δ-mediated mechanism54, it is perhaps not surprising that gender differences were observed in this study. The gene discussed is AR; the disease is Familial prostate cancer.