Motorneurons from transgenic mice lacking the GEF Plekhg5 and in which Rab26 activation is deficient show accumulation of SV proteins and enlarged SVs that result in motorneuron disease [72], indicating that both Rab26 and Plekhg5 participate in the autophagy-dependent degradation of SVs. This evidence concerns the gene PLEKHG5 and motor neuron disorder.