To test whether prolonged upregulation of Mettl3 in the NOD mouse β-cells would lead to a faster turnover and/or decrease in expression of Oas and delay T1D progression we designed two different adeno-associated virus serotype 8 (AAV8) driving eGFP or Mettl3 under the control of the rat insulin promoter II (RIP2)47 (Fig. 7a and Extended Data Fig. 7a). The gene discussed is METTL3; the disease is type 1 diabetes mellitus.