The study demonstrated that pre-T2D, not T2D ASCs, compared to non-diabetic, had exhibited a substantial decrease in levels of mesenchymal markers CD90 and CD105, and in response to IL-1β stimulation, they significantly increased the gene expression of COX-2 and Forkhead box G1 (FOXG1) and the secretion of PGE2. The gene discussed is THY1; the disease is type 2 diabetes mellitus.