Combined with our previous finding that NF-κB P65 could directly mediate the transcription of CXCL16 in keratinocytes through directly binding to the promotor of CXCL1645, we draw a conclusion that CXCL16 is mainly elaborated by IRF3 and NF-κB in the downstream of MAVS under virus infection. Here, IRF3 is linked to viral infectious disease.