Since T2D are complex conditions where sub-acute and chronic inflammation plays a crucial role via the production of pro-inflammatory cytokines and activation of major inflammatory pathways, particularly TNF-α and NF-κB56,57, our findings suggest that Sam68 may provide a mechanistic link between tissue inflammation and the pathophysiology of diabetic hyperglycemia. Here, KHDRBS1 is linked to type 2 diabetes mellitus.