This is even more true given the availability of personalized therapies; examples are the new drugs used in SMA [104,105], or the identification of the presence of the C9orf72 hexanucleotide repeat expansion or SOD1 mutations in ALS as a necessary criterion for enrollment into clinical trials for antisense oligonucleotide (ASO) therapy [7]. This evidence concerns the gene SOD1 and proximal spinal muscular atrophy.