However, it has been reported in transgenic mouse models that, when AR inhibitors were used to treat PC cells with TP53 and RB1 gene loss, these cells gained CSC, epithelial-to-mesenchymal, basal, and neuroendocrine phenotypes through the action of transcriptional factors, such as SOX2, and, later, developed into NEPC [15]. The gene discussed is AR; the disease is pachyonychia congenita.