ACSL4 have been shown to drive ferroptosis by activating and facilitating the incorporation of PUFAs into membrane lipids (for example, phospholipids), whereas CV‐6 utilizes ACSL4 to manipulate lipid metabolism to promote the formation of viral replication organelle.[19] Considering IAV as an enveloped virus utilizing large amounts of lipids as vesicles and energy sources.[53] Combined with metabolomics, it was shown that IAV remodeled the lipid metabolism of host cells after infection. This evidence concerns the gene ACSL4 and infection.