These results are consistent with those of Kochi and Xiao, who suggested that EGCG reduces the severity of liver injury in an experimental model of NAFLD and is associated with lower concentrations of pro-fibrogenic molecules, reactive oxygen species, and pro-inflammatory mediators by modulating TGF/SMAD, PI3K/Akt/FoxO1, and NF-κB signaling (28, 56). The gene discussed is AKT1; the disease is metabolic dysfunction-associated steatotic liver disease.