Defective mitochondrial transport in axons has been linked to both developmental and late-onset neurological disorders. Axonal trafficking is in large part governed by two motors traveling along microtubules: kinesin-1 and cytoplasmic dynein 1 (dynein). Dynein is the primary retrograde transport motor in axons, and mutations in dynein and many of its regulators also cause neurological diseases. One of dynein's most famous regulators, LIS1,  is especially important in adult neurons. Its deletion in adult mice leads to severe neurological phenotypes, demonstrating crucial post-developmental functions. While LIS1 is known to stimulate the retrograde transport of acidic organelles in cultured adult sensory axons, its role in mitochondrial transport remains uncharacterized. In their new study titled "LIS1 and NDEL1 Regulate Axonal Trafficking of Mitochondria in Mature Neurons", members of the Smith lab report a novel function of LIS1 and its protein partner NDEL1 in regulating mitochondrial dynamics in adult axons, raising the possibility that defects in the LIS1/NDEL1 dynein regulatory pathway could contribute to mitochondrial diseases with axonal pathologies. Nice work!