ATAC‐Seq results revealed that with PCa progression, transcriptional activation of AR target genes, such as KLK2, KLK3, and FKBP5, changed remarkably and correlated with the AR transcriptional program (Figure S3A–C, Supporting Information), whereas patients with CRPC had more accessible chromatin at the KLK11 and AMACR locus (Figure 2I,J). The gene discussed is AR; the disease is posterior cortical atrophy.