It has been reported that persistent interferon signalling orchestrates PDL1-dependent and PDL1-independent resistance to ICB.34 So, for most studies have been focused on IFNγ-induced PDL1 expression,35,36 but there were distinct biological functions between IFNγ and IFNα in tumour immunology.37 Therefore, our study is of great significance since it is the first to demonstrate that IFNα can strongly promote the transcriptional expression of PDL1 and the formation of an immunosuppressive microenvironment through IFNAR1 in HNSCC. The gene discussed is CD274; the disease is neoplasm.