These findings support the role of Slug as a key transcriptional regulator of these changes51 and are supported by animal models and limited human explant studies.56 We show that adaptation and survival appear to be the default state, with tumor regression being associated with the selective depletion of vulnerable cells defined by loss of SNAI2. These findings indicate that SNAI2 has potential as a predictive biomarker of response to AR-targeting drugs and that agents targeting SNAI2 expression would be expected to augment therapeutic response. The gene discussed is AR; the disease is neoplasm.