PAK3 and hereditary spastic paraplegia: This presynaptic phenotype produced by the loss-of-function of D-Spastin is recovered when the actin cytoskeleton-regulator protein p21-activated kinase 3 (pak3) is also down-regulated, since the aberrant diffuse MTs observed at distal tips of presynaptic terminals at NMJs of D-Spastin null Drosophila is recovered in animals that lack both pak3 and D-Spastin (Ozdowski et al., 2011), raising the possibility that combined regulation of actin and MT cytoskeleton dynamics could be concertedly controlled in the development of the HSP disease.