In conclusion, while several different pathways could lead secondarily to atlastin-associated disease, the ability to catalyze membrane fusion is the only function demonstrated for atlastin(s) to date and evidence-based mechanistic links between fusion and other proposed disease pathways leading to HSP have not been corroborated making defects in membrane fusion the most likely route to SPG3A disease. The gene discussed is ATL1; the disease is hereditary spastic paraplegia.