While insulins and SLC5A11 appear to be key players in glucose-responsive feeding, it is quite likely that other cumulative changes, triggered by the hyperglycemia, contribute to the observed feeding defect; in the fly there is substantial and complex crosstalk occurring between the brain and non-IPC insulins, Akh, NPF, sNPF, hugin, drosulfakinin, dopamine etc33,45,48. The gene discussed is SLC5A11; the disease is Hyperglycemia.