The importance of this axis has been clarified through TLR4 mutant mice resistant to the development of NAFLD [50]; furthermore, a direct link between TLR4 and Kupffer cells was described in the pathogenesis of steatohepatitis, as the experimental destruction of Kupffer cells was shown to prevent the increased expression of TLR4 [51]. The gene discussed is TLR4; the disease is metabolic dysfunction-associated steatotic liver disease.