Other non-genetically induced mild SMA models include suboptimal dosing with AAV9-SMN (Meyer et al, 2015), oligonucleotides targeting SMN splicing (Zhou et al, 2015; Osman et al, 2016), and AAV-9s targeting disease-modifying proteins such as plastin-3 (Kaifer et al, 2017) and follistatin (Feng et al, 2016). The gene discussed is SMN1; the disease is proximal spinal muscular atrophy.