Several studies support this hypothesis: In a 70–90 weeks study, Lee al. showed that rAAV‐G6PC‐mediated gene therapy expressed 3%–63% of wild‐type hepatic G6Pase‐a activity in G6pc−/− mice, maintaining glucose hemostasis and preventing chronic HCA formation.7, 31. The gene discussed is G6PC1; the disease is hepatocellular adenoma.