Bothtumor tissue and mammary gland demonstrate a higher expression of IR and increasedphosphorylation of the IR/IGF-1R and Akt; furthermore, administration of pharmacologicalblockers of IR and IGF-1R specifically abrogates the accelerated tumor growth.9 In conclusion, this study suggestedthat the IR/IGF-1Rs are the mediators of the tumor-promoting activity ofhyperinsulinemia. Here, INSR is linked to neoplasm.