Using histone H3 lysine4 methylation as an indicator of transcription activation to further dissect the mechanism, we found that H3K4me2 was highly enriched around ARE2, but not ARE1 in PCa C4-2 cells, and this enrichment was much more obvious upon Enz treatment, indicating a negative autoregulation of AR transcription in the PCa cells (Fig. 2E). This evidence concerns the gene AR and posterior cortical atrophy.