Based on the relation between acute Nod1 signalling and prominent features of metabolic disease, and the ability of TKIs to inhibit Ripk2, we hypothesized that: (1) Ripk2 was required for Nod1-mediated immunometabolism effects, (2) TKIs that inhibit Ripk2 would lower Nod1-ligand induced lipolysis, inflammation and dysglycemia. The gene discussed is NOD1; the disease is Other metabolic disease.