Altogether, these studies pinpoint three important things—(i) a possible underlying gain-of-toxic-function mechanism by the C9orf72 astrocytes in ALS/FTD pathogenesis, (ii) a level of toxicity related to possible direct physical communication between C9orf72 astrocytes and neurons or secretion of possible neurotoxic agents from C9orf72 astrocytes, and (iii) an impaired capacity of C9orf72 astrocytes to support neurons. This evidence concerns the gene C9orf72 and frontotemporal dementia.