Moreover, it is apparent that in addition to correcting insulin resistance, NPC43 can cooperate with insulin to further inhibit hepatic gluconeogenesis and stimulate liver glucose uptake, as indicated by the more conspicuous decrease in G6pc expression and the more evident increase in glucose uptake in mouse liver AML-12 cells after co-treatment with NPC43 and insulin rather than NPC43 or insulin alone (Figs. 3b, 5c). The gene discussed is INS; the disease is Insulin resistance.