The silencing of pro‐oncogenic risk factors of HNSCC such as MUC4 or FXR1 induces senescence in HNSCC cells through activation of the p16/Rb or p53/p21 pathway, respectively.15, 16 On the other hands, the re‐activation of tumour suppressor proteins including Myb‐binding protein 1A (MYPPB1A) or Fbxo4 as well as miRNAs such as miR‐34a or miR‐494‐3p which are suppressed in HNSCC tissues was shown to promote cell cycle arrest and senescence and enhance radiosensitivity in HNSCC cells.17, 18, 19, 20. This evidence concerns the gene TP53 and head and neck squamous cell carcinoma.