For example, studies have shown that N-glycosylation of programmed death ligand 1 (PD-L1) prevents phosphorylation-dependent proteasomal degradation by glycogen synthase kinase-3 β (GSK3β) and β -transducin repeat-containing proteins (β-TrCP) while promoting its stability and interaction with PD-1 to enable tumor immune evasion, with epidermal growth factor (EGF) signaling further stabilizing PD-L1 through GSK3β inactivation23,24,25. The gene discussed is EGF; the disease is neoplasm.