In preclinical models, androgen deprivation therapy (ADT) reduces copper levels in prostate cancer cells by downregulating CTR1 expression.3 However, castration-resistant cells often exhibit reactivated AR signaling (e.g., via AR-V7) and restored copper metabolism, contributing to therapy resistance.4 For example, Gao et al.18 showed that enzalutamide, an AR antagonist, increases mitochondrial dependence in CRPC cells, sensitizing them to copper ionophore-induced cuproptosis.18 This suggests that targeting the androgen-copper axis may overcome resistance in advanced disease. Here, AR is linked to prostate carcinoma.