Spinal muscular atrophy(SMA),as a serious hereditary neuromuscular disease,is caused by pathogenic mutations in the survival motor neuron 1(SMN1)gene,leading to a deficiency in the encoded product,survival motor neuron(SMN)protein.Clinical treatment of SMA has long been a challenging issue in the medical field.After detailed clinical observation and electrophysiological testing,we found that the administration of nosina-cin sodium in SMA patients significantly increased the expression of full-length SMN protein in muscles,thereby optimizing the transport efficiency of neuromuscular junctions and enhancing muscle contractile function.In addi-tion,the drug can regulate nerve excitability,increase nerve conduction speed,promote muscle regeneration,and further improve the electrophysiological performance of patients,bring hope to the treatment of SMA patients.