Furthermore, we showed that TMUB1 induced PD-L1 stability by regulating the post-translational modifications of PD-L1, protecting it from binding to HUWE1, and recruiting STT3A to promote PD-L1 glycosylation, thereby saving it from ERAD degradation, and promoting tumor growth in vivo by facilitating PD-L1-mediated immune evasion. The gene discussed is CD274; the disease is neoplasm.