Nevertheless, the activation of a canonical-like WNT/CTNNB1 pathway by virus infection must play its regulatory role in the late stage of IRF3 transcriptional activity in the infected cells via different scenario for a CTNNB1-IRF3 protein complex: import inhibition into the nucleus, increased nuclear export, increased protein degradation or as repressor of transcription. This evidence concerns the gene IRF3 and viral infectious disease.