Patients with CRPC develop resistance arising from multiple molecular mechanisms, such as increased androgen biosynthesis in the tumour microenvironment or through alterations of AR signalling, including AR mutations, constitutively active AR variants in the absence of ligands, AR gene amplifications, use of other signalling pathways or reliance on non-AR-mediated pathways [3, 5, 6]. The gene discussed is AR; the disease is neoplasm.