This raises the question, whether (a) fatty liver is quantitatively linked to fasting glucagon secretion and hepatic GCGN resistance in T2DM as reflected by elevated fasting AA and the GCGN–alanine index and (b), whether a reduction of liver fat would improve the hepatic GCGN resistance in people with T2DM as might be expected if NAFLD is a primary cause of hyperglucagonemia. This evidence concerns the gene GCG and type 2 diabetes mellitus.