These findings are not only consistent with results of previous studies but also extend them.23,24,25 Analyzing the Dallas Heart Study and the Dallas Biobank, the Copenhagen City Heart Study, and the Copenhagen General Population Study populations, Stender et al23 reported a synergistic interaction between BMI and nonalcoholic fatty liver disease–related single-nucleotide variants (PNPLA3 I148M, TM6SF2 E167K, and GCKR P446L) in affecting hepatic triglyceride content, liver enzymes, and cirrhosis. The gene discussed is GCKR; the disease is Cirrhosis.