Since collateral activation of IGF1R (implicated in increased cancer rates) is a key concern in the use of insulin or insulin analogs for the treatment of diabetes [35–37] and quinone-containing and polyphenolic insulin mimetics, such as DAQ-B1 and 6CI-TGQ, were previously reported to either activate or interact with IGF1R [14, 16], we performed a detailed analysis of activation status of endogenous Igf1r in liver and skeletal muscle of Leprdb/db mice following daily i.p. NPC43 treatment for 52 days. The gene discussed is INS; the disease is cancer.