In addition, an adaptive increase in AR expression and AR copy number gain has also been observed in circulating tumor cells (CTCs) as well as cell-free circulating tumor DNA (ctDNA) from patients with CRPC receiving next-generation AR-directed therapies (i.e., abiraterone and enzalutamide)—implicating this as mechanism by which cell growth can escape the inhibitory effects of these drugs [9, 11, 33, 34]. The gene discussed is AR; the disease is neoplasm.