On the basis of the high hepcidin levels found in the three experimental groups with a leaner phenotype, Tmprss6−/−and both iron-treated Tmprss6−/−and Tmprss6+/+ mice, we further investigated whether hepcidin up-regulation might be responsible for the induction of lipolysis and the HFD-obesity resistance phenotype observed in matriptase-2 deficient mice. The gene discussed is HAMP; the disease is obesity due to melanocortin 4 receptor deficiency.