It must be pointed out that some of the beneficial effects of butyrate administration were statistically significant in in vivo and in vitro experiments; however, SCFA treatment did not totally reverse T2D-induced renal dysfunction, and high glucose-induced oxidative stress and NF-κB activation were not totally inhibited by SCFAs or a GPR43 agonist, suggesting the presence of other mechanisms, such as the inhibition of HDAC, which are involved in the crosstalk of SCFAs and the kidney in the prevention and treatment of DN [8, 28, 29]. This evidence concerns the gene NFKB1 and liver dysplastic nodule.