To address this hypothesis, we aimed at comparing infection-induced type I IFN production in 1) a condition of TBK1 deficiency in which IKKε is upregulated (TBK1-depleted cells) with 2) a condition of TBK1 deficiency in which IKKε is not upregulated (TBK1-depleted cells expressing inactive TBK1 K38A or S172A). The gene discussed is TBK1; the disease is infection.