While ALD and NAFLD exhibit largely conserved pathophysiological implications, several divergent molecular pathways have been identified: In macrophage, MyD88 is recruited to Toll-like receptor 4 (TLR4) upon ligand binding and then activates downstream signaling in NASH, while MyD88 seems not to be involved in TLR4 signaling in ASH [42,53,54]. Here, MYD88 is linked to metabolic dysfunction-associated steatotic liver disease.