We hypothesize that differential expression of the ChREBP–PPARα–FGF21 axis across liver, subcutaneous, and omental adipose tissues could distinguish metabolic conditions (MHL, MHO, MUL, and MUO) and correlate with hepatic histopathological changes and biochemical indicators of metabolic dysfunction, thereby contributing to the variability and progression of MASLD. This evidence concerns the gene MLXIPL and metabolic dysfunction-associated steatotic liver disease.