-TBK1 has been associated with autoimmune diseases such as systemic lupus erythematosus (SLE), where dysregulated immune responses contribute to tissue damage and inflammation. TBK1 may play a role in the activation of immune cells and the production of inflammatory cytokines in autoimmune conditions. TBK1 is also responsible for regulating the immune response in multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, and psoriasis among others -There is growing evidence linking TBK1 dysfunction to neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Mutations in the TBK1 gene have been identified in individuals with ALS-FTD spectrum disorders, suggesting a potential role for TBK1 in the pathogenesis of these diseases. -TBK1 is involved in the host immune response to viral infections by inducing the production of type I interferons and other antiviral proteins. Dysregulation of TBK1 signaling pathways may impact the ability of the immune system to control viral infections, leading to increased susceptibility to viral diseases. -TBK1 has been implicated in cancer development and progression in various ways. It can promote tumor growth, survival, and metastasis by enhancing cell proliferation, inhibiting apoptosis, and modulating the tumor microenvironment. Dysregulated TBK1 signaling has been observed in several types of cancer, including lung cancer, breast cancer, and melanoma. For instance, TBK1 has been shown to activate the NF-κB pathway, which is generally involved in inflammation, cell proliferation, and resistance to apoptosis in cells. This can eventually lead to tumor growth and proliferation. TBK1 phosphorylates STING, which in turn recruits IRF3 for phosphorylation by TBK1. Phosphorylated IRF3 dimerizes and then enters the nucleus, where it functions with NF-kB to turn on the expression of type I interferons and other immunomodulatory molecules. TBK1 activates several signaling pathways such as AKT-mTOR and MYC that are responsible for tumor cell survival. TBK1 also plays an important role in the IRF3 pathway that is important in generating an antiviral response, any disruption in these pathways is linked to tumorigenesis. In addition, TBK1 is also known to activate transcription factors responsible for epithelial-mesenchymal transition (EMT) which can lead to cancer metastasis. It can also influence the tumor microenvironment by modulating immune cell activity and causing cytokine release which can cause tumor progression. It is also implicated in resistance to different cancer therapies as it can inhibit apoptosis and promote cancer cell survival. TBK1 is also involved in crosstalk between other cancer-linked pathways in the cell such as KRAS, PI3K, and EGFR pathway. Due to all these factors any mutation inTBK1 gene can be linked to cancer.