Coherently, we found that viral infection induces the accumulation of an active form of CTNNB1 and that CTNNB1 gene silencing increases SeV-induced IFNB1, IFIT1 and TNF expression, as well as NFKBIA (IκBα) phosphorylation at serine 32 (P-Ser32) to release NF-κB inhibition. Here, CTNNB1 is linked to viral infectious disease.