More recent evidence has emerged from studies of C9orf72-null mice, which display an age-related inflammatory response in macrophages and microglia, suggesting that loss of C9orf72 protein could potentially contribute in a non-cell autonomous manner to the neurodegeneration observed in patients with ALS/FTD (O’Rourke et al., 2016). The gene discussed is C9orf72; the disease is frontotemporal dementia.