Another study by Miller et al. showed that Tau phosphorylation mediates abnormalities observed in motor neurons since expressing phosphorylation-mimetic Tau forms leads to motor axon abnormalities, while non-phosphorylatable Tau forms rescue motor axon phenotype in smn-MO zebrafish, indicating that hyperphosphorylation of Tau, as in many neurodegenerative disorders, is also involved in SMA [47]. This evidence concerns the gene SMN1 and proximal spinal muscular atrophy.