Given that overexpression of ATF6 in the livers of obese animals seems advantageous in reversing the effects of CRTC2 on the gluconeogenic program, this interaction between ATF6 and CRTC2 may be a significant factor in the impairment of hepatic gluconeogenesis in obesity and type 2 diabetes.5 Here, CRTC2 is linked to obesity due to melanocortin 4 receptor deficiency.