We know that some malignant tumors secrete excessive insulin-like substances, namely, insulin-like growth factor (IGF-I and IGF-II), because IGF is structurally homologous to insulin and can interact with IGF-I and IGF-II, which are insulin receptors that exert endogenous insulin-like effects.[3] However, the patient’s IGF-I results were normal, so this possibility was excluded. The gene discussed is INS; the disease is cancer.