Macrophages and dendritic cells (DC) have been shown to produce the majority of type I IFN following in vivo infection with L. monocytogenes [18, 19], which can act by autocrine or paracrine signaling via the IFNαβR, culminating in the activation of signal transducer and activation of transcription (STAT)-1/STAT-2 intracellular signaling pathways [20]. The gene discussed is IFNAR2; the disease is infection.