Very recently, ChREBP was proposed to contribute to the development of diabetic nephropathy through the induction of HIF1-α in glomerular mesangial cells [20,21] In the pancreatic β-cell, ChREBP activation by high glucose results in increases in triglyceride content and a reduction in glucose-stimulated insulin secretion [9,13]. The gene discussed is INS; the disease is diabetic kidney disease.