Increased G6P and F26BP activate transcriptional activity of ChREBP/Mlx in hepatocytes and, through this, increased expression of glycolytic, gluconeogenic, and lipogenic genes, which contributes to hepatic steatosis and insulin resistance—including increased expression and activity of ChREBPβ [73,77,82]. The gene discussed is MLXIPL; the disease is Hepatic steatosis.