As recently demonstrated by Safi and colleagues, even if low levels of systemic or intratumorally produced androgens can facilitate the control of prostate cancer growth and progression as a first-stage approach, a paradoxical mechanism of high dose androgens also exhibits considerable efficacy as a treatment modality in late-stage metastatic prostate cancer, facilitating the formation of AR dimers/oligomers to suppress c-MYC expression, and inhibiting proliferation (Safi et al. 2024). The gene discussed is AR; the disease is Familial prostate cancer.