Consistent with previous report that adenovirus-mediated IRF-3 transgene expression changed the microglial cytokine profile from a proinflammatory phenotype to an anti-inflammatory phenotype [46], our data in human NSCLC cells showed that specific knockdown for hnRNP A1/A2 or SF2/ASF could contribute to forming a proinflammatory cytokine milieu through regulating IRF-3 splicing pattern and expression of downstream effector molecules. Here, IRF3 is linked to non-small cell lung carcinoma.