Compared to MAVS-ΔN141, these chimeric mutants MAVS-ΔN141-(Bcl-xL-TM) and MAVS-ΔN141-(VAMP-2-TM) lost their inhibitory effects on IFN production and MAVS aggregation upon virus infection (Supplementary Fig. 3a,b), though they contain active regions for interaction with downstream effectors. The gene discussed is IFNA1; the disease is viral infectious disease.