For example, p53 deacetylation can reduce acute kidney injury caused by sepsis by promoting autophagy,[59] and SIRT1‐mediated HMGB1 deacetylation can inhibit sepsis‐related acute kidney injury.[60] Recently, novel lysine acylation reactions, including propionylation, butyrylation, malonylation, succinylation, crotonylation, 2‐hydroxy‐butyrylation, β‐hydroxy‐butyrylation, glutarylation, and lactylation, have been extensively examined. This evidence concerns the gene TP53 and acute kidney injury.