More recently the heterozygous A1AT Pi*MZ phenotype has been recognized as an important disease modifier in patients with metabolic syndrome–associated fatty liver disease, and alcohol-associated fatty liver disease.1 Studies have shown that heterozygous A1AT Pi*MZ phenotype increases the risk of developing cirrhosis and hepatic decompensation in patients with metabolic syndrome–associated fatty liver disease,1–3 It is thus essential to determine if a patient with chronic liver disease carries the Pi*MZ phenotype. This evidence concerns the gene SERPINA1 and fatty liver disease.