Wu et al. (2017) reported a novel protective locus for SMA patients, the A-G transition at the –44 position on SMN2 intron 6, which disrupted the original HuR-dependent ISS and increased the inclusion of exon 7 of SMN2. Moreover, altered expression of some genetic modifiers, such as plastin 3 (PLS3) and neurocalcin delta (NCALD), also possibly improves the clinical phenotype of SMA patients (Oprea et al., 2008; Riessland et al., 2017). This evidence concerns the gene PLS3 and proximal spinal muscular atrophy.