IGF1R and Hyperglycemia: Given the increased expression IR-A within neoplastic tissues and preferential affect upon IGF-induced mitogenic signaling, as opposed to IR-B that exerts greater influence upon glucose hemostasis within normal liver, muscle and fat, one could conceivably target just IGF-1R and the oncogenic IR-A splice variant while minimizing hyperglycemia and untoward side effects associated with down-regulated IR-B.