In this setting, we can foresee two scenarios: in miR‐9 low tumors, the addition of CTX to RT, via blockage of the EGFR signaling pathway, will further decrease miR‐9 expression, eventually contributing to the effectiveness of RT treatment; in miR‐9 high tumors, the EGFR signaling pathway inhibition by CTX is not sufficient to dampen the miR‐9/KLF5/Sp1 axis and HNSCC will resist to treatments and eventually progress. This evidence concerns the gene EGFR and head and neck squamous cell carcinoma.