In addition, we generated in vivo Drosophila models of WS by generating mutants of fly homologs of human WFS1 and CISD2, dWFS1, and dCISD, respectively, and observed diabetes-like phenotypes that resemble major human WS symptoms that were rescued by IP3R overexpression, demonstrating that restoring calcium homeostasis can alleviate WS-related diabetic complications. The gene discussed is ITPR1; the disease is Werner syndrome.