Shiet al. [62] discovered that TMUB1 enhances the N-glycosylation of PD-L1 by recruiting STT3A and subsequently enhancing its stability, thus promoting PD-L1 maturation and tumor immune evasion, and they also synthesized a competitive small-molecule polypeptide PTPR, which effectively inhibits the binding of PD-L1 to TMUB1, thereby exerting an antitumor effect by reducing the abundance of PD-L1 via N-glycosylation. This evidence concerns the gene CD274 and neoplasm.