Specifically, we confirmed that deletion of tbcm significantly increased the expression of genes related to mitochondrial dysfunction, such as TRIM39 and SARM1, until 4 h postinfection, which is a relatively early stage of infection, and suppressed the expression of SLC25A26, NDUFA8 and DTYMK, which are associated with maintaining mitochondrial homeostasis (Fig. 4C). The gene discussed is SARM1; the disease is infection.