While further studies are necessary to inquire which endogenous HO product, CO or biliverdin/bilirubin, is responsible for attenuation of obesity in vivo58, the current observation showing crucial roles of heme-mediated PGRMC1 dimerization led us to suggest that CO serves as a modulator of adipogenesis to inhibit plasma membrane translocation of LDL/VLDL-R and GLUT4 by dissociating the heme-mediated dimer. The gene discussed is SLC2A4; the disease is obesity due to melanocortin 4 receptor deficiency.