Since p53, STAT3 and NF-κB phosphorylation at individual sites is associated with their activation and the pathogenesis of AKI, it is anticipated that administration with AZ505 may improve kidney function and minimize tubular cell injury through inhibiting H3K36me3-mediated gene transcription as well as regulating phosphorylation of these non-histone proteins (see below). This evidence concerns the gene NFKB1 and acute kidney injury.