We found that infection of macrophages with the classical RIPK1/caspase-8–activating pathogen, Yptb, sensitized TBK1/IKKε-inhibited cells to enhance RIPK1/caspase-8 activation and death (Fig. 3, F and G), likely due to the reported direct inhibitory phosphorylation of RIPK1 by TBK1 (3, 4), but also to enhance secondary caspase-1 activation. The gene discussed is IKBKE; the disease is infection.