In this work, we demonstrated for the first time that silencing hnRNP A1/A2 or SF2/ASF in human NSCLC cells increased exclusion of exons 2 and 3 of IRF-3 gene and reduced expression levels of IRF-3 protein and IRF-3 downstream effector molecules IFNβ and IP-10, which further influence cytokine production and contribute to forming a proinflammation cytokine milieu in human NSCLC/PBMC co-cultures. The gene discussed is IFNB1; the disease is non-small cell lung carcinoma.