Mechanistically, circCLMP shielded IRF3 from binding to TBK1, interfered with the phosphorylation and nuclear translocation of IRF3, thereby inhibiting the activation of interferon response, suppressing CD8<sup>+</sup> T cell infiltration in the tumor environment, and eventually mediating immune evasion and promoting the progression of MSI tumors. This evidence concerns the gene TBK1 and neoplasm.