Moreover, deletion of Mid1 decreased susceptibility of mice to viral myocarditis, pneumonia, and herpes simplex encephalitis by enhancing the production of type I IFN through its interaction with protein phosphatase 1A (PPM1A) responsible for dephosphorylation of TANK binding kinase 1 (TBK1). This evidence concerns the gene TBK1 and susceptibility to pneumonia measurement.