Examples include (i) FOXM1-PROTAC, which degrades FOXM1 (Forkhead box protein M1), reducing GLUT1 (Glucose transporter 1) and PD-L1 (Programmed death-ligand 1) expression and resulting in cancer suppression; (ii) AR pep-PROTAC, which lowers AR (androgen receptor) levels and induces tumor regression; and (iii) xStAx-VHLL, which promotes human β-catenin degradation and hinders Wnt signaling pathway-dependent tumor growth [23]. The gene discussed is AR; the disease is neoplasm.