Conrad et al. also elucidated the essential role of the GSH/GPX4 axis in preventing lipid‐oxidation‐induced acute renal failure and ferroptotic cell death using inducible GPX4(‐/‐) mice.[25] Our research suggests that Snord3a inhibits the normal biology of GPX4 and ACSL4 in lipid metabolism, leading to lipid peroxides accumulation and GSH depletion. This evidence concerns the gene ACSL4 and acute kidney injury.