Together these findings suggest that post-natal AAV9-mediated SMN1 delivery may not rectify all the dysregulated proteins found in the Smn2B/− mouse model of SMA, and as these proteins have the potential to detrimentally impact heart function, additional cardiac monitoring may prove useful in the long-term care of SMA patients. The gene discussed is SMN1; the disease is proximal spinal muscular atrophy.