Subsequent studies showed that the two ADAR1 isoforms act in an opposite manner, with p110 acting as an antiviral factor, restricting IAV replication, whereas p150 instead enhances replication because of its ability to suppress IFN-beta and RIG-I-like receptor signaling, the latter of which is thought to be a part of the broader role of p150 in preventing hyperactivation of the innate immune response during viral infections (Heraud-Farlow and Walkley 2020; Vogel et al. 2020). This evidence concerns the gene ADAR and viral infectious disease.