The primary mechanisms of therapy resistance include AR alterations (AR splice variants, mutations, amplifications), a shift to AR-independent growth, overexpression of efflux transporters such as P-glycoprotein, alterations in tubulin dynamics, epithelial-to-mesenchymal transition (EMT), modifications to the tumor microenvironment, as well as activation of pro-survival pathways, including PI3K/AKT/mTOR, JAK/STAT, and TGF-β5. This evidence concerns the gene AR and neoplasm.