These observations may be of interest for the pathophysiology of hepatic steatosis that is described by increased plasma glucagon concentrations [29] and increased hepatic lipid flux [45]; these ‘dual-hit’ signals may offer an explanation as to why CEACAM1 expression [46] and ICR [8, 31] are reduced in people with increased liver fat. This evidence concerns the gene CEACAM1 and fatty liver disease.