Furthermore, we show that the lack of mitochondrial fragmentation in infected si-Mic10 cells is not a consequence of the reduced infection efficiency, as wild-type cells challenged with noninvasive bacteria lacking internalins A and B (ΔinlAB) (Fig. S3A) displayed mitochondrial fragmentation levels comparable to those seen with wild-type Listeria-infected cells (Fig. S3B and C), as well as increased mitochondrial Mic10 levels similar to what we observed in wild-type Listeria-infected and LLO-treated cells (Fig. S3D). The gene discussed is MICOS10; the disease is infection.