As expected, among the CRPC genes, the ones upregulated in Adeno- vs. NE-CRPC contributed to androgen resistance toward the aberrant AR signalling pathway, while neuroendocrine transdifferentiation was sustained by increased EZH2 and HES6 expression, promoting androgen independence and the neuroendocrine phenotype acquisition of PCa cells [2,88,90]. The gene discussed is AR; the disease is posterior cortical atrophy.