The TLR4/MYD88/NF-κB signaling axis has been proven to be of great significance in self-tumor cell clearance and autoimmune diseases.62,63 PDTC were selected as the NF-κB inhibitor, which can inhibit the phosphorylation of IκB, and prevent the translocation of NF-κB into the nucleus.64 MYD88 is the canonical adapter for inflammatory signaling pathways that is present downstream of the TLR and IL-1 receptor families, and it is the central node of the inflammatory pathway.65 Therefore, we used MYD88-KO mice for BCP implant experiments, as they are widely used for such studies.66–68. The gene discussed is NFKB1; the disease is neoplasm.