Our data indicating a type I IFN–independent role for MDA5 in the innate immune response to M. tuberculosis are consistent with previous reports demonstrating a type I IFN–independent function for MDA5 in other disease states, namely the antiviral response to Sendai virus infection (50) and the mitochondrial apoptosis pathway in melanoma cells (51). The gene discussed is IFIH1; the disease is melanoma.