Of note, although EREG and EGF are both EGFR ligands, their mechanisms in activating EGFR signaling are different.38 In HNSCC, EREG promotes tumor progression by inducing c-Myc expression, and Myc regulates PDL1 expression at the transcriptional level.24 Thus, the finding of this study, stabilized EREG via N-glycosylation, provides novel mechanism of PDL1 upregulation for immunoevasion in HNSCC. The gene discussed is EGF; the disease is neoplasm.