In head-and-neck cancer, HPV-positive tumors exhibited an almost complete mutual exclusivity with mutations in known drivers such as TP53, CDKN2A and TERT (FDR-corrected P = 1.73 × 10−5, 1.73 × 10−5 and 0.012, respectively; multiple testing corrected for presented mutations in EBV and HPV, DISCOVER22) (Fig. 3c, Supplementary Table 13), as reported previously25, which could be explained by the mutation-independent inactivation of TP53 due to the human papillomaviruses28,29,30. The gene discussed is TP53; the disease is malignant tumor of neck.