Niebler et al., showed that infection of primary keratinocytes with HPV16 E6, but not E7, abrogated IL‐1β processing and secretion in a proteasome‐dependent manner that was mediated by ubiquitin ligase E6‐AP and p53.35 The authors further suggest that continual IL‐1β ablation leads to complete loss of IL‐1β gene altogether as HPV‐mediated malignancy develops.35 It is tempting to speculate that a similar mechanism also exists in HPV‐positive OPC cells and this may explain the difference in IL‐1β expression between in vitro cultured HPV‐positive and HPV‐negative OPC cells observed in our study. This evidence concerns the gene TP53 and infection.