Despite these convincing studies with the K. pneumoniae strain, it has been suggested that increased ethanol levels in patients with NAFLD may be due to insulin-dependent impairments of the alcohol dehydrogenase pathway rather than an increase in endogenous alcohol production from the gut.85 Thus, endogenous ethanol production by gut microbiota seems very likely to be one of the major culprits in the development of liver steatosis in some, but surely not all NAFLD patients. This evidence concerns the gene INS and metabolic dysfunction-associated steatotic liver disease.