We mated Lcn2 Tg mice with Lcn2 KO mice under C57BL/6 J genetic background and observed that obesity resistance in Lcn2 KO mice under HFD was completely rescued in Lcn2 KO-Tg mice (Fig. 5), suggesting that activities of LCN2 protein upon energy homeostasis and metabolism were exerted in an endocrine manner24. The gene discussed is LCN2; the disease is obesity due to melanocortin 4 receptor deficiency.