It would be intriguing to examine creatine uptake and whether localization of PKCδ within a higher molecular weight complex in mitochondria is impaired in cells of multi-system mitochondrial disease patients with CL synthase (CRLS1) dysfunction in which loss of CL and phosphatidylglycerol accumulation results in fragmented mitochondrial morphology and bioenergetic dysfunction[30]. Here, PRKCD is linked to inborn mitochondrial metabolism disorder.