HES6 and posterior cortical atrophy: 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].