One possible explanation of this discrepancy is that while TP53 mutations are widespread amongst the tumor mass due to its contribution to initiation and subsequent progression of HNSCC cases associated with classical risk factors, TP53 mutant cell clones in HPV-associated HNSCC cases may be more limited, in some cases amounting to just 1–10% of the tumor mass. This evidence concerns the gene TP53 and neoplasm.