It also identified the kinases that contribute to the reduced insulin-stimulated phosphorylations in T2D, including a reduction in the activity of AKT2, as well as reductions in AMPKA2, MAPKAPK2, PHKG2, and some less-studied kinases with regard to insulin action, including YANK3/STK32c, BRSK2, TTBK2, and WNK3. Here, PRKAA2 is linked to type 2 diabetes mellitus.