In support of this possibility, it has been shown that mice with liver specific deletion of the IGF-I gene exhibited elevated GH levels, which were associated with insulin resistance and impaired activation of early signaling events in response to insulin.[3] It has been demonstrated that blocking of GH action in mice with liver specific deletion of the IGF-I gene by crossing them with mice over-expressing a mutant form of GH, which prevents GH activation of its receptor, results in improved insulin sensitivity. Here, INS is linked to Insulin resistance.