Further studies revealed that TBK1 promoted the establishment of inflammatory TME by activating the NF-κB signaling pathway, increasing the release of inflammatory cytokines (type I interferon, IL-6, and IL-17) from HCC cells, recruiting TAMs, and inhibiting the activation of tumor-infiltrating CD8+ T cells [12,13]. The gene discussed is NFKB1; the disease is neoplasm.