Notably, we also found that in response to androgens, in two independent prostate cancer models, there was a dynamic re-organization of H2A.Zac at AR enhancers to promote RNA pol II recruitment and transcription of eRNAs before gene activation, demonstrating that H2A.Zac plays a critical role in priming the functional activity of enhancers essential for oncogene expression. Here, AR is linked to prostate cancer.