These data and the observation of Ca2+-dysregulations in growth cones of Smn-deficient motoneurons in cell culture [139] and in vivo in neuromuscular endplates [260, 291, 292] support the hypothesis that Ca2+-dependent F-actin bundling could be a specific target for therapy development in SMA, in particular during early/prenatal development stages of the neuromuscular endplate. This evidence concerns the gene SMN1 and proximal spinal muscular atrophy.