The importance of cellular excitability for motoneuron survival and function is strengthened by recent reports on the voltage-gated sodium channel Nav1.9 which significantly contributes to motoneuron axon growth on laminin-111 (Subramanian et al., 2012; Wetzel et al., 2013) and the loss of the potassium channels Kv2.1 which corresponds to motoneuron degeneration in SMA mouse models (Fletcher et al., 2017). The gene discussed is KCNA3; the disease is proximal spinal muscular atrophy.