However, regarding the involvement of Notch signaling in pancreatic β-cells, a recent study demonstrated that a blockade of DLL/Notch signaling by antibodies against DLL4 protected islets and β-cell homeostasis and reversed diabetes in nonobese diabetic mice (T1DM spontaneous model) and STZ-treated mice and promoted differentiation and proliferation from pancreatic progenitor cells to insulin-producing cells in wild-type mice [97]. The gene discussed is INS; the disease is type 1 diabetes mellitus.