It is known the blockade of IGF-1R enhances GH levels to induce hyperglycemia,33 but hyperinsulinemia is also seen.34 Studies have suggested that individual tumors may rely upon IR signaling for growth and proliferation.35, 36 In tumors where IR has a pathophysiologic role, anti-IGF-1R mAbs would not be expected to confer a clinical benefit if elevated insulin levels and IR activation are a result of the anti-IGF-1R therapy. Here, IGF1R is linked to hyperinsulinism.