2020). Furthermore, in fecal samples of diabetic rats, excessive acetate disrupted cholesterol homeostasis by activating GPR43, leading to tubulointerstitial injury in DKD (Hu et al. 2020). A previous study also reported that acetate promoted podocyte injury by stimulating GPR43 activation and inhibiting Akt signaling (Lu et al. 2021). In contrast, in GPR109A-/- diabetic mice, GPR109A deletion did not play a critical role in maintaining intestinal homeostasis (Snelson et al. 2020). The gene discussed is AKT1; the disease is diabetic kidney disease.