(1): Oral–gut portal route: periodontitis increases the swallowing of oral bacterial taxa and LPS [53]; in NAFLD/MASLD, increased intestinal permeability facilitates LPS translocation, permitting transcellular absorption into the portal vein via lipid rafts and CD36 (with a smaller contribution via chylomicrons), while chylomicron-mediated postprandial transport further augments endotoxin flux to the liver [54]. This evidence concerns the gene CD36 and metabolic dysfunction-associated steatotic liver disease.