AR and neoplasm: To date, AR-V7 synthesis, upregulation of CYP17 and/or alteration in AR signaling axis, expression of glucocorticoid receptor (GR), upregulation of PI3K/AKT/MAPK and/or GATA2 signaling, altered tumor microenvironment, and deregulation of microRNAs (miRNAs) have been considered as possible mechanisms involved in the acquired resistance to Enz and Abi [4,17,18].