In addition to a maladaptive role for ChREBP in promoting excessive glucose production, three out of four liver-selective ChREBP loss-of-function studies show that hepatic ChREBP is essential for the development of obesity, hyperinsulinemia, and systemic insulin resistance (Fig. 3A) (79, 80, 81, 82). The gene discussed is MLXIPL; the disease is Hyperinsulinemia.