Although RNAs have historically been considered the principal stimuli for IFN-α and IFN-β production by activating IRF3 through retinoic acid­inducible gene I (RIG-I)-like receptors (RLRs) or toll-like receptors (such as TLR3, TLR7) during antiviral immune responses, tumor-derived RNA is only minimally stimulatory in growing tumors [18]. Here, IFNA1 is linked to neoplasm.