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This classification transcends the traditional dichotomy between metabolic and toxic etiologies, acknowledging the synergistic nature of the interactions between metabolic dysfunction and alcohol exposure [7]
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In contrast, mutant TP53 has been proved to drive the glycolysis by activating the RhoA/ROCK/GLUT1 signaling cascade (164), repress the catabolic activities, such as fatty acid oxidation (FAO), by inhibiting 5′-AMP-activated protein kinase (AMPK) pathways, and enhance the anabolic processes, such as enhanced fatty acid synthesis (174)
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