Finally, as demonstrated in children with NAFLD, OSA could induce liver damage by increasing intestinal permeability and endotoxemia, that in turn activate Kupffer and hepatic stellate cells, and by expanding adiponectin-deficient hepatic progenitor cells, key features of steatohepatitis and fibrosis [52]. This evidence concerns the gene ADIPOQ and metabolic dysfunction-associated steatotic liver disease.