These results indicate that ferroptotic stress is well controlled in macrophages upon bacterial infection, i.e., by increasing ferrous iron levels at the early stage of infection via pro-ferroptotic pathways (e.g., Nrf2/HO-1 and ferritin/NCOA-4 axes), retaining intracellular ferrous iron by reducing FPN-mediated efflux, and protecting cells from ferroptotic damage by instigating anti-ferroptotic pathways (e.g., GPX4 expression) (Figure 6L, Video S1). Here, GPX4 is linked to bacterial infectious disease.