AKT1 and metabolic dysfunction-associated steatotic liver disease: This well-defined PTEN/PI3K/AKT pathway allows clear mechanistic studies compared to the complex, poorly characterized effects of dietary components [25]; (3) PTEN knockout produces consistent, reproducible metabolic phenotypes unaffected by feeding variations among individual mouse [26]; (4) Western diets can reduce PTEN expression, so PTEN knockout reliably recapitulates Western diet effects [27]; 5) clinical MASLD/MASH biopsies show PTEN downregulation and concurrent hyperactivation of AKT, making this model more translationally relevant [27].