To gain insight into the function and regulation of MAVS following RLR activation, we investigated the kinetics of signaling downstream of RIG-I by infecting HEK293T or HeLa cells with the Sendaï virus (SeV) H4 strain [8], a strain composed mostly of small, copy-back defective interfering genomes and whose infection overproduces short uncapped 5'-triphosphate RNAs that are specific ligands for RIG-I [2]. The gene discussed is RIGI; the disease is infection.