The role of HATs in diabetic nephropathy has been recently reviewed by Li et al. (11) and provides evidence that high glucose-induced increased activity and levels of HATs, such as p300, CBP, and p/CAF, are mediating the activation of pro-inflammatory cytokines, ECM proteins, endothelial function, and fibrotic processes in diabetic nephropathy, via acetylation of both histone and non-histone proteins, such as Smads, p53, SP1, and NF-κB. Here, NFKB1 is linked to diabetic kidney disease.