The difference in prognosis is at least partly due to the increased radio/chemosensitivity of HPV+ve tumours [13], but there also other major biological differences between these tumour subtypes, with HPV+ve tumours commonly retaining wild-type p53 and Rb gene modulation and showing an absence of field cancerisation and an increased host adaptive immune responses; all subjects of recent research [14,15,16]. The gene discussed is RB1; the disease is neoplasm.