The findings indicate that PRC2 functions chronically in β cells, that PRC2-insufficiency contributes to the pathology of human T2D, and, therefore, that inhibition of PRC2-opposing factors (e.g., Mll, Jmjd3, and Utx) might serve as potential therapeutic strategy for T2D. This evidence concerns the gene KDM6B and type 2 diabetes mellitus.