Therefore, while we cannot completely exclude the possibility of C9orf72 haploinsufficiency affecting autophagy, our results suggest that although C9orf72 clearly is an important player in the endolysosomal pathway and possibly other vesicle trafficking pathways, C9orf72 haploinsufficiency is highly unlikely to be the primary driving force behind the autophagic defects observed in MNs from C9orf72 ALS/FTD patients. The gene discussed is C9orf72; the disease is frontotemporal dementia.