Despite these questions, studies of host metabolism collectively support that mouse adipose ILC2s regulate insulin sensitivity of the adipose tissue by production of IL-5 and IL-13, whereas group 1 ILCs may play a detrimental role in mammalian obesity through proinflammatory macrophage polarization and promotion of tissue fibrosis. The gene discussed is IL5; the disease is obesity due to melanocortin 4 receptor deficiency.