Additional, SMN-independent curative approaches to SMA have been proposed, namely, inhibition of myostatin, negative regulator of muscle growth by Apitegromab, restoration of mitochondrial function by Edaravone levetiracetam, reduction of excitotoxicity in microenvironment by Riluzole/gabapentin, activation of fast troponin to increase muscle force by Reldesemtiv, inhibition of Acetylcholinesterase to improve function of neuro-muscular junctions by Pyridostigmine, and others (summarized in [69]). The gene discussed is SMN1; the disease is proximal spinal muscular atrophy.