Studies have shown that the genetic susceptibility resulting from TBK1 heterozygosity can be exacerbated by the decrease of TGFβ-activated kinase 1 (TAK1) expression in the aging-induced brain, thereby promoting receptor-interacting protein kinase 1 (RIPK1) and activating ALS/FTD [115]. This evidence concerns the gene TBK1 and frontotemporal dementia.