The involvement of TBK1 mutations in neuroinflammation during ALS relies on the removal of T cells protective regulation (due to the ability of CD4+ cells in stabilizing microglial activation, decreasing pro-inflammatory cytokines, and increasing growth factor IGF-1) observed in both the spinal cord lesions of ALS patients and TBK1 knockout mice, leading to a decrease in T cell number in the CNS [33]. Here, IGF1 is linked to amyotrophic lateral sclerosis.