This hypothesis is in line with the reported long time lag (from 15 to 30 years) between an oral HPV infection and the development of HPV-related OSCC, and with the reported major impact of p16INK4a expression on response to treatment and overall survival of patients with head and neck cancer treated using conventional radiotherapy.87,88 Low levels of PARP-1 and CAF-1/p60 with the absence of a significant number of HPV-positive tumour cells showing a CSC phenotype could therefore explain the reduced DNA-repair ability and radioresistance that characterizes this subgroup of OSCCs. Here, PARP1 is linked to neoplasm.