The axonal hits include, for example, the Ephrin receptor EPHA4, a component of NMJ [74] whose knockout causes motor deficits in mice [75]; the choline transporter SLC5A7, mutated in hereditary motor neuropathies [76]; laminin A (LAMA1) whose neuronal knockdown results in abnormal morphology and neurite formation [77]; laminin B (LAMB1) whose mutation in mice leads to dystonia-like movement disorders with spinal defects [78]; and heparan sulfate proteoglycan 2 (HSPG2), which is aberrantly spliced in MNs of ALS patients [79] and associated with tardive dyskinesia [80] (Fig. 6B). Here, HSPG2 is linked to movement disorder.