While the results obtained from the SMNΔ7mouse model afforded important insights into the dynamics of gene- and exon-level expression changes over time, to ensure that our findings were not restricted to this particular transgenic model of SMA, but applicable to SMA mouse models in general, we performed a similar analysis on the more severe but genetically less complicated Smn−/−;SMN2 mouse model of SMA [32]. This evidence concerns the gene SMN1 and proximal spinal muscular atrophy.