We found that, upon infection with S. aureus, ACO2 KD further increased the expression of HSPD1, HSPA9, and CLIPP, three of four selected targets of ATF5, a key mediator of the UPRmt and the mammalian ortholog of C. elegans ATFS-1, in HeLa cells (Supplementary Fig. 12h–j). The gene discussed is ACO2; the disease is infection.