Elevated TREX1 expression has been observed in HPV-associated cervical cancer, facilitating tumor proliferation and progression by impeding p53 functionality.37 Furthermore, TREX1 also acts as a safeguard mechanism; under high IR doses, it is activated to degrade cytosolic DNA and thereby preventing activation of cytosolic DNA sensing pathway and subsequent immune response.28,38 We hypothesize that activation of cytosolic DNA sensors in HPV16-related OPSCC is influenced by both HPV16 oncoproteins E6 and E7 as well as TREX1. The gene discussed is TP53; the disease is neoplasm.