In 2012, Corti and colleagues showed that the transplantation of SMA hiPSC-derived MNs, previously corrected in vitro with single-stranded oligonucleotides to convert a SMN2 into a SMN1-like gene, into the SpC of newborn SMA mice modestly ameliorated disease phenotype and increased the mouse lifespan [170]. Here, SMN1 is linked to proximal spinal muscular atrophy.