One good example is how androgen receptor (AR)-targeted therapy in metastatic PC can result in short-term tumour suppression effects but also induces castrate-resistant PC (CRPC) in the long term that presents an AR-indifferent phenotype containing weakly expressed AR and AR-regulated PSA, cancer stem cell (CSC) markers (e.g., CD44, CD133, BMI1, EZH2), and even AR negative neuroendocrine PC (NEPC) markers (e.g., CHGA, SYP) [5,6,7]. This evidence concerns the gene BMI1 and pachyonychia congenita.