For example, PTEN deficiency in glioblastoma mediate PDL1 upregulation through the PI3K-AKT pathway.6 In lung cancer, EGFR mutations are closely associated with PDL1 dysregulation.7,8 However, EGFR mutations are extremely rare in HNSCC, whereas upregulation of wild-type EGFR is prevalent in about 80 to 90% of HNSCCs.9 These suggest that the mechanisms underlying dysregulated PDL1 in HNSCC are different from those in lung cancer. This evidence concerns the gene AKT1 and lung cancer.