MTOR and Rett syndrome: Our evidence has revealed that MeCP2 promotes miR-199a processing as a Drosha complex component at the post-transcriptional level and miR-199a elevates mTOR signaling activity, which is implicated in a variety of neurodevelopmental and psychiatric diseases [94], by repressing expression of mTOR signaling inhibitors including Sirt1, Hif1α, and Pde4d. Also, we have shown that the genetic deletion of miR-199a recapitulates many phenotypes of RTT model mice.