However, it is also important to take into account the role of germline, somatic, or epigenetic mutations as new, promising, molecular networks and signaling pathways implicated in aggressive PC, such as STAT3, PTEN, ATM, AR, and P53 [30], or cfDNA (cell free DNA) and exosome-RNA, as reliable sources of AR variants, and their combined detection in liquid biopsy that predicts resistance to AR signaling inhibitors in PC [31]. The gene discussed is AR; the disease is pachyonychia congenita.