Several taxa have been found to be associated with NAFLD, and the reviews addressing the role of GM and metabolites in NAFLD as well as it interventions can be found elsewhere; potential pathways appear to be through microbial LPS, altered intestinal permeability, TMAO, and secondary bile acids and their receptors such as FXR (Figure 2B) [54,108,109]. This evidence concerns the gene NR1H4 and metabolic dysfunction-associated steatotic liver disease.