Moreover, we demonstrate that DR3 engagement induces both the canonical and/or non-canonical NF-κB pathways in naïve and activated ILC2s as evidenced by upregulation of p52, p65, NIK (encoded by Map3k14), Nfkb2, and Relb. Using a DR3 specific agonist antibody, we establish that DR3 engagement on ILC2s both protects against the development of T2DM and is capable of reversing already established T2DM. The gene discussed is TNFRSF25; the disease is type 2 diabetes mellitus.