Co-regulator modification (e.g., GRHL2) [25], co-transcriptional R-loops-mediated epigenetic regulation [26], and intratumoral steroid synthesis, mainly androgens, after androgen deprivation therapy play a critical role in metastatic castration-resistant PCa (mCRPC) progression [27], and androgen promiscuity, the situation in which mutated androgen receptors may be activated by alternative ligands, including estrogen and other hormones [28,29,30], which contribute to the progression and pathogenesis of PCa (Figure 4). The gene discussed is AR; the disease is posterior cortical atrophy.