This paradoxical outcome aligns with clinical and experimental studies showing that advanced MASLD progression is driven not by triglyceride accumulation, but by lipotoxicity from alternative lipid mediators (diacylglycerols [DAGs], ceramides) and impaired lipid-handling mechanisms, including reduced VLDLR expression, which limits lipid uptake but exacerbates lipotoxic stress and hepatocellular injury [51,52,53,54]. This evidence concerns the gene VLDLR and metabolic dysfunction-associated steatotic liver disease.