Interestingly, controlled knockdown of SMN in neonatal mice induced a severe neuromuscular disease phenotype, whereas the depletion of SMN after P17 in mice (when the fully NMJ maturation is established) had relatively low effect: moreover in adult SMN-depleted mice, a selective NMJ pathology occurred only in aged or injured animals. This evidence concerns the gene SMN1 and neuromuscular disease.