With pituitary-gonadal axis suppression by ADT, circulating levels of testosterone and DHT decline dramatically; however, tumor growth can persist through persistent exposure of the prostate to intratumoral androgens derived from either adrenocortical precursor steroids or de novo synthesis from cholesterol.18 In 2013, Chang and colleagues4 identified that a minor allele in HSD3B1 conferred a novel resistance mechanism to ADT. This evidence concerns the gene HSD3B1 and neoplasm.