Diminished levels of survival motor neuron protein (SMN) cause motor neuron dysfunction and muscle wasting in spinal muscular atrophy (SMA), and there is evidence that the therapeutic restoration of SMN is effective in treating this disorder. However, we still have little understanding of how SMN maintains neuromuscular function and how its loss drives SMA. Kim, Jha et al. now provide new insight into this issue, revealing evidence that SMN has a specific role in the assembly of the synaptic SNARE complex at neuromuscular junctions (NMJs).