Additionally, systemic administration of antisense oligonucleotides (ASO) targeting an SMN2 intronic splicing silencer on PND 1 dramatically prolongs the lifespan of SMA mice, even though inclusion of exon 7 significantly decreased after PND 30 [28], suggesting that transiently increasing SMN protein levels during the first few weeks has beneficial effects on long-term survival of SMA mice. The gene discussed is SMN2; the disease is proximal spinal muscular atrophy.