Mutations in the genes coding for axonal transport first came to light when LaMonte et al. showed that disruption of the dynein/dynactin interaction by postnatal overexpression of p50/dynamitin, a 50-kDa subunit of dynactin encoded by DCTN2, caused reduced axonal transport in motor neurons and consequently led to a late-onset progressive motor neuron disease phenotype in the transgenic mice [82]. The gene discussed is DCTN2; the disease is motor neuron disorder.