Such mechanisms comprise: (1) steroidogenesis upregulation within the prostate tumor, allowing the synthesis of endogenous androgens [20,73,74]; (2) higher AR expression in prostate tumor cells, mainly due to AR gene amplification [22]; (3) single point mutations within AR gene LBD [75,76,77]; (4) silencing through methylation of the gene encoding the androgen-inactivation enzyme HSD17B2 [78]; (5) variants of the HSD3B1 gene [79]; (6) upregulation of the glucocorticoid receptor [80], and (7) emergence of AR splice variants. This evidence concerns the gene HSD17B2 and prostate neoplasm.