While our results do not support the hypothesis that widespread, systematic splicing abnormalities cause SMA, we cannot rule out the possibility that splicing of one or several transcripts is critically affected by SMN deficiency, and that the few splicing changes observed early in our mice contribute to SMA pathogenesis, followed by a cascade of loss of splicing fidelity or secondary effects. The gene discussed is SMN1; the disease is proximal spinal muscular atrophy.