Furthermore, results of the present study also suggest that TLR1 may also be a critical factor in the development of NAFLD and that a genetic deletion of this receptor dampens the development of NAFLD; however, it remains to be determined, if these beneficial effects depend upon a decreased sensitivity towards LTA or other bacterial toxins and if effects alike are also found in humans. Here, TLR1 is linked to metabolic dysfunction-associated steatotic liver disease.