Studies have shown that inhibition of STAT3 leads to increased phosphorylation of p65 and NF-κB, as well as enhanced infiltration of T cells, resulting in impaired tumor growth and robust immune responses.148 Owing to the phosphorylation, transcriptional activity, and translocation ability of interferon regulatory factor 3 being inhibited by its binding with E6, the downstream expression of IFNβ is suppressed, which facilitates HPV to evade immune responses.149. The gene discussed is NFKB1; the disease is neoplasm.