These findings again correspond with the findings in human C9orf72 neurons, showing a similar increased susceptibility to glutamate-induced toxicity, providing support for the validity of the NCS34 cells expressing (G4C2)106 or (G4C2)288 as a cellular model to study the toxicity of HRE which is known to be of utmost importance in C9orf72 ALS-FTD related mechanisms [13]. The gene discussed is C9orf72; the disease is frontotemporal dementia.