An explanation for this paradox lies in the heterogeneityof prostate tumors, which develop resistance to AR inhibition throughdiverse mechanisms including upregulation of AR-V7 (an AR splice-variantwith constitutive transcriptional activity that lacks a ligand-bindingdomain) and glucocorticoid receptor (GR).63−65 Both AR-V7and GR signaling drive increased KLK2 and KLK3 expression even inthe face of Enz treatment. This evidence concerns the gene AR and prostate neoplasm.