We found enhancer-binding transcription factor-addicted cancers (for example, AR–FOXA1-driven prostate cancer) to be exquisitely and preferentially sensitive to SWI/SNF ATPase degradation, which triggered an instantaneous, specific loss of physical accessibility and transcription factor binding at enhancer elements, thereby disrupting enhancer-wired oncogenic gene programs. The gene discussed is FOXA1; the disease is cancer.