It would also be interesting to develop a more in-depth understanding of the precise histone acetylation sites targeted by the individual HDAC inhibitors that are crucial for radiosensitisation and DSB repair inhibition, as well as the specific mechanism linking these events (such as altered chromatin accessibility or DNA repair protein expression) in order to appreciate the full therapeutic potential of HDAC inhibition for the radiosensitisation of HNSCC. This evidence concerns the gene HDAC9 and head and neck squamous cell carcinoma.