AR and neoplasm: Whilst the use of AR inhibitors are now amongst the primary options for androgen-targeted therapies in early-stage prostate cancers (45, 46), these options become ineffective once the tumor becomes castrate-resistant, as they are able to circumvent androgen targeted treatments via various mechanisms which include AR amplification, point mutation, splicing variants and replacing AR functions with glucocorticoid receptors (4, 47, 48).