Carcinogenic factors N-MYC, AURKA [19,56], and MUC1-C [21], loss of tumor suppressors PTEN, RB1, and TP53 [22], and amplification of epigenetic controls and transcriptional factors like FOXA1 [23], FOXA2 [24], EZH2 [20], REST [30], and BRN2 [41] have the potential to drive PCa/CRPC transformation into NEPC. The gene discussed is FOXA2; the disease is posterior cortical atrophy.