According to a model based on a concentration dependent biphasic switch, at early stages of infection low levels of LGP2 would enhance MDA5-mediated antiviral signaling, but as infection progresses and LGP2 production is induced by IFN, LGP2 would act as a negative feedback regulator inhibiting MDA5 signaling [7–9]. The gene discussed is IFIH1; the disease is infection.