We have previously reported that deletion of Smad3 from db/db mice (Smad3 KO‐db/db) completely protects against the development of the type‐2 diabetic phenotype including the obesity, hyperglycaemia, hyperlipidaemia, and importantly, the glucose intolerance and insulin resistance by largely improving islet β‐cell functions.19 This evidence concerns the gene SMAD3 and obesity disorder.