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MASH\u2010associated liver fibrosis develops through a complex interplay among lipotoxic hepatocyte injury, oxidative and endoplasmic reticulum stress, inflammatory macrophage activation, hepatic stellate cell (HSC) activation and excessive extracellular matrix (ECM) deposition. E3 ubiquitin ligases, which determine substrate specificity within the ubiquitin\u2010proteasome system, have emerged as important regulators of these processes. By controlling protein stability, signalling complex formation, inflammatory responses, cellular stress, autophagy, ferroptosis and intercellular communication, E3 ubiquitin ligases can influence both fibrosis progression and resolution. Because E3 ubiquitin ligases may exert pro\u2010fibrotic or anti\u2010fibrotic effects depending on the substrate, cell types, metabolic environment and disease stage, their therapeutic targeting requires disease\u2010 and cell type\u2010specific strategies. 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