It is becoming apparent from these Drosophila studies into human MND that mutations of fly homologues of VAPB [270], SMN [275], NIPA1 and Spastin [286, 287] all seem to activate the same pathogenic pathway, suggesting that de-regulated BMP type II receptor signalling may unify ALS, SMA and HSP. The gene discussed is VAPB; the disease is amyotrophic lateral sclerosis.