Additionally, alternative mechanisms independent of AR, such as abnormal hormonal secretion in the tumor microenvironment, DNA damage repair (DDR), phosphoinositide 3-kinase–protein kinase B–mammalian target of rapamycin (PI3K–AKT–mTOR), and Wnt–β-catenin, play critical roles in the development of ADT resistance [12–14]. This evidence concerns the gene AKT1 and neoplasm.