The observed slightly detrimental effect of macroH2A1.2 overexpression on lipid and glucose metabolism in vitro is consistent with the upregulation of macroH2A1.2 observed in vivo [21]; however it is not known if this upregulation of macroH2A1.2 observed in the livers of mice models of NAFLD is consequent to lipid accumulation or to other disease factors (oxidative stress, inflammation) that in turn could trigger NAFLD causatively through macroH2A1.2 upregulation. This evidence concerns the gene MACROH2A1 and metabolic dysfunction-associated steatotic liver disease.