In mouse models of spinal muscular atrophy (SMA), deficiency of SMN protein leads to an accumulation of miR-183 and other miRNAs in the axon, and axonal synthesis of mTOR protein is impaired, leading to reduced mTORC1 and mTORC2 signaling and reduced axon outgrowth. This evidence concerns the gene MTOR and proximal spinal muscular atrophy.