In parallel, there is a decrease in the expression of the endogenous RIPK1 inhibitor TANK-binding kinase 1 (TBK1), which leads to neuroinflammation, additional TDP-43 aggregation, axonal degeneration, loss of neurons and behavioral deficits, and the further manifestation of signs of ALS and FTD (Freischmidt et al., 2017). This evidence concerns the gene TBK1 and amyotrophic lateral sclerosis.