Amongst these, we focused on KIF5A for an in-depth study for multiple reasons: their presence and function have not been previously described in astrocytes; neuronal kinesin-1/KIF5A dysfunction has been implicated in a broad range of diseases caused by KIF5A-mutations, including ALS15,16, Charcot-Marie-Tooth type 2 disease (CMT2) and hereditary spastic paraplegia (HSP)33,34; kinesin1/KIF5A-related perturbations can also occur in non-KIF5A mutation-related ALS forms21,22. This evidence concerns the gene KIF5A and Charcot-Marie-Tooth disease type 2.