Finally, we show that the TNF-α/SETDB2 pathway is upregulated in T2D wound fibroblasts and that fibroblast-specific knockdown of Setdb2 or pharmacologic inhibition of JAK1,3/STAT3 improves wound healing in diabetic mice and leads to increased myofibroblast gene expression in T2D wounds. The gene discussed is JAK1; the disease is type 2 diabetes mellitus.