Due to these data, in context with a growing appreciation that mitochondrial dysfunction may play a role in RTT, and because anaplerotic diet therapy has aided a wide range of metabolic diseases, we hypothesized that there may be a deficit in general fuel substrate utilization in Mecp2 KO, irrespective of specific derangements, that could benefit from anaplerotic therapy using triheptanoin. This evidence concerns the gene MECP2 and Other metabolic disease.