On the other side of the coin, the upregulated expression and activity of estrogen receptor-α (ERα) and ERα‐regulated genes (e.g., MAPK, PI3K, the TMPRSS2‐ERG fusion, and NEAT1) during the progression of PCa to CRPC suggests that tumors can bypass the AR signaling axis by using estrogens for their growth (7–9). The gene discussed is AR; the disease is posterior cortical atrophy.