PC progression is a multistep process, starting with prostatic intraepithelial neoplasia, advancing to localized castration-sensitive PC (CSPC), progressing to castration-resistant PC (CRPC) by losing the androgen receptor (AR) dependency, then developing into advanced mCRPC with local invasion and metastatic lesions, and finally exerting neuroendocrine transdifferentiation, driven by neuronal transcription factors to the poorly treatable neuroendocrine PC phenotype [2]. The gene discussed is AR; the disease is pachyonychia congenita.