For immune surveillance in HCC, various PRRs, such as cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) (5), retinoic acid-inducible gene I (RIG-I) (6), and Toll-like receptors (TLRs) (7), can favor the transcription of pro-inflammatory genes via pathways involving interferon regulatory factor 3 (IRF-3) and nuclear factor kappa B (NF-κB), inducing the production of interferons (IFNs), cytokines, and chemokines and ultimately potentiating cytotoxic anti-tumor responses mediated by effector T and NK cells. The gene discussed is IRF3; the disease is neoplasm.