In glioma cells, the presence of constitutive interferon beta promoted immune escape by upregulating PDL1.13 Here, we show that endogenous IFNα signalling is constitutively active in HNSCC, and that IFNα can promote PDL1 expression through IFNAR1/Stat1 signalling in HNSCC. This evidence concerns the gene IFNAR1 and glioma.