Moreover, the down-regulation of the lipolytic program to wild-type levels, together with the recovery of the fat mass and the increased weight gain observed in anti-HJV-treated Tmprss6−/−mice, further supports the promoting role of hepcidin and lipolysis in the obesity-resistant phenotype of matriptase-2 deficient mice. The gene discussed is TMPRSS6; the disease is obesity due to melanocortin 4 receptor deficiency.