The energetic regulation of LE/Lys plus-end transport mediated by CPT1C seems to be of particular importance for corticospinal neurons, the ones with longer axons in the body, since individuals carrying the missense CPT1CR37C or the nonsense CPT1CQ76X mutations develop HSP (Hong et al., 2019; Rinaldi et al., 2015). This evidence concerns the gene CPT1C and hereditary spastic paraplegia.