EGCG mitigates liver steatosis in MAFLD by enhancing lipid metabolism through the adiponectin and SIRT1–LKB1–AMPK signaling pathways. EGCG facilitates an increase in adiponectin levels by inhibiting the phosphorylation of ERK1/2. This increase allows PPARγ to bind to the PPRE located in the promoter region of target genes, thereby influencing adiponectin transcription. Once in the bloodstream, adiponectin is transported to the liver, activating the AdipoR2, which activates SIRT1. This activation leads to the phosphorylation of LKB1 and its subsequent translocation from the nucleus of hepatocytes to the cytoplasm. Consequently, phosphorylation of AMPKα occurs, which in turn influences the expression of key regulators of lipid metabolism genes, including SREBP1c, ChREBP, ACC, and FAS. EGCG = epigallocatechin-3-gallate; ERK1/2 = extracellular signal-regulated kinase 1/2; PPARγ = peroxisome proliferator-activated receptor γ; PPRE = peroxisome proliferator response element; AdipoR2 = adiponectin receptor 2; SIRT1 = sirtuin 1; LKB1 = liver kinase B1; AMPK = AMP-activated protein kinase; SREBP1c = sterol regulatory element-binding protein 1c; ChREBP = carbohydrate response element-binding protein; ACC = acetyl-CoA carboxylase; FAS = fatty acid synthase.