Thus, it is likely that under diabetic conditions, deregulated metabolic signaling (e.g., glucagon and insulin) result in skewed posttranscriptional modifications and subcellular trafficking of Sam68 to increase CRTC2 stability, and studies to identify these site-specific modifications may provide additional mechanistic insights and therapeutic targets of T2D. This evidence concerns the gene KHDRBS1 and type 2 diabetes mellitus.