PRRT2 and Insulin resistance: Insulin resistance condition activated PKCδ, PKCθ, and GSK3β, resulting in phosphorylation of insulin receptor substrate (IRS) proteins and attenuating insulin signaling.15, 16, 17 miR-26a directly repressed PKCδ, PKCθ, and GSK3β expression, which contributed to the positive role of miR-26a in insulin signaling.