PRRT2 and Hyperglycemia: Since PKC activation plays a major role in the intracellular signaling leading to oxidative stress, cell dysfunction and tissue damage in hyperglycemia, and is required for p66Shc translocation to mitochondria in response to stress (70), it is tempting to hypothesize that p66Shc may play a role in cardiovascular complications induced by hyperglycemia acting as a downstream target following high glucose-induced PKCβ activation.