The idea that prostate cancer cells can be driven toward androgen independence via the pathway of drug-induced epigenomic plasticity which reprograms circadian rhythm regulation has recently been explored in a phase 2 clinical trial by Linder et al. This study demonstrated that in tissues of patients with high-risk prostate cancer treated with 3 months of enzalutamide monotherapy, there was reprogramming in pioneer factor forkhead box protein A1 (FOXA1), which ultimately led to these FOXA1 sites being enriched for the circadian clock component BMAL1. Here, BMAL1 is linked to prostate carcinoma.