HSP patient-derived cells had 50% the control level of spastin, a tubulin-severing enzyme, 150% of the control level of stathmin, a tubulin depolymerizing enzyme, and 50% of the control level of acetylated a-tubulin, an indicator of stabilized microtubules (Abrahamsen et al., 2013). This evidence concerns the gene SPAST and hereditary spastic paraplegia.