Overexpression of MCCC1 potentiated virus-triggered activation of the IFN and pro-inflammatory cytokine promoters and induction of the endogenous IFN and pro-inflammatory cytokine genes, whereas MCCC1 knockdown had the opposite effect, suggesting that MCCC1 is an important component of innate immune signaling pathways in response to viral infection. The gene discussed is MCCC1; the disease is viral infectious disease.