In zebrafish models of SMA generated by antisense morpholinos or maternal zygotic genetic mutations (Hao et al., 2013; McWhorter et al., 2003), developing motor axons and dendrites display outgrowth and branching defects, whereas in mouse and human, SMA motor axons correctly reach the target muscle and form the NMJ, followed by denervation of the muscle as the disease progresses (Ling et al., 2012). This evidence concerns the gene SMN1 and proximal spinal muscular atrophy.