Interestingly, gut lymphocyte homing is a process involved in NAFLD pathogenesis, as has been shown in the experimental NASH model where MAdCAM-1 deficiency improved the disease (130); therefore, further research aimed at evaluating the pharmacological modulation of gut lymphocyte homing as a therapeutic strategy is needed. This evidence concerns the gene MADCAM1 and metabolic dysfunction-associated steatotic liver disease.