To investigate the effect of the T1D pathophysiological inflammatory milieu on ADAR1 and the β cell transcriptome, we have analyzed high-throughput RNA sequencing data from human islets and EndoC-βH1 cells exposed to IFNα or IFNγ/IL1β, cytokines that contribute to the pathogenesis of T1D (16, 17). The gene discussed is IFNG; the disease is type 1 diabetes mellitus.