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). The gene discussed is AR; the disease is prostate cancer.