Given the critical role of the FKBP52 proline‐rich loop that overhangs the PPIase pocket in the regulation of AR activity (Storer Samaniego et al., 2015), we speculate that ID4 could target distinct regulatory sites within FKBP52 for the disruption of AR signaling in PCa. The gene discussed is FKBP1A; the disease is posterior cortical atrophy.