Previous studies have reported that the tumor PD-L1 level can be regulated at the transcriptional level (eg, via EGFR, the MAPK pathway, Janus kinase-signal transducer and activator of transcription pathway, nuclear factor kappa-B (NF-κB) pathway, hypoxia-inducible factor-1α, MYC, Anaplastic lymphoma kinase, Met, BRD4),46 and via post-translational modification (eg, via CDK4, B3GNT3, GSK3β, CSN5, CMTM4, and CMTM6).47 In this study, we revealed that UBQLN4 interacts with PD-L1 and stabilizes the PD-L1 protein. The gene discussed is ALK; the disease is neoplasm.