Mechanistically, MTHFD2 promotes the production of uridine diphosphate N-acetylglucosamine (UDP-GlcNAc), leading to O-GlcNAcylation of MYC, a post-translational modification (PTM), that results in its stabilization, and the subsequent increased expression of programmed cell death 1 ligand 1 (PD-L1), thereby blocking anti-tumor immune responses [35]. The gene discussed is MYC; the disease is neoplasm.