The highly durable nature of this inhibitory effect, combined with evidence linking NPY/AgRP neuron activation to the pathogenesis of hyperglycemia in diabetic animals, offers a potentially novel, feasible, and testable mechanism to explain sustained glucose-lowering elicited by i.c.v. FGF1 injection in murine models of T2D. The gene discussed is FGF1; the disease is type 2 diabetes mellitus.