Equally, whether PLS3 overexpression has been achieved genetically from a transgene or from AAV9-expressing PLS3 cDNA, it led to improved motor neuron axon outgrowth and NMJ functionality, extension of survival and motoric ability especially in low-dose SMN-ASO treated severe SMA mouse models [18, 19, 21, 54]. This evidence concerns the gene SMN2 and proximal spinal muscular atrophy.