Such a pharmacological inhibition of β-cell ncNOS activity was now found to restore the impaired insulin response to glucose and also to restore, at least in part, the increase glucagons secretion in GK islets thus suggesting that the increased NO generation in these islets is indeed an important factor for β-cell dysfunction and α-cell hyper-responsiveness in this model of animal type 2 diabetes. The gene discussed is INS; the disease is type 2 diabetes mellitus.