Our results, showing impaired Rb pathway (loss of expression of RB1 and/or of CDKN2A) in 55.9% of analysed cases confirmed the hypothesis that RB1 pathway (55.9%) is commonly disrupted in HNSCC development and progression, with CDKN2A (45%), rather than RB1 (11.8%) being the frequent direct target for inactivation (Lang et al, 2002). Here, RB1 is linked to head and neck squamous cell carcinoma.