Several studies that include animal models [3–5], human fluid biomarkers [6–8], or brain tissue immunohistochemistry [9–11] have provided evidence that an ongoing inflammatory process is involved in the progression of sporadic or genetic FTD, manifesting as microglial activation/dystrophy, astrogliosis, and increased secretion of inflammatory markers, including tumour necrosis factor (TNF) and interleukin (IL) cytokines [12, 13]. The gene discussed is TNF; the disease is frontotemporal dementia.