The current study shows that normalization of hepatic ChREBP activity in GSD Ia liver induces progressive and extreme dysplastic liver growth, hepatocyte hypertrophy and -proliferation, YAP activation, cholestasis, CIN, DNA damage, cGAS-STING pathway activation, inflammation, cellular senescence, and hepatocellular dedifferentiation. The gene discussed is MLXIPL; the disease is cervical squamous intraepithelial neoplasia.