Importantly, our study provides a mechanistic explanation for the previously unexplained observation that patients with point mutations in TBK1 that lead to kinase deficiency are highly susceptible to severe viral infection, while patients completely lacking TBK1 expression are not (24, 25): Kinase-dead TBK1 mutants are still capable of inducing the degradation of IKKε, as demonstrated for TBK1 K38A and TBK1 S172A in this study. The gene discussed is TBK1; the disease is viral infectious disease.