AR and prostate neoplasm: There are several mechanisms by which prostate tumours may reactivate androgen signalling, including gain-of-function mutations or alternative splicing of the androgen receptor (AR) that broaden its range of ligands to other steroid hormones (e.g., progesterone, estrogen, and cortisol), antiandrogens (e.g., flutamide and bicalutamide) [114–116], or confer ligand-independent activity [117].