A common immunopathogenic mechanism across many of these cancers is the activation of the MyD88/NF‐κB axis, which drives the secretion of pro‐inflammatory cytokines (e.g., IL‐6, TNF‐α), promotes angiogenesis, and upregulates anti‐apoptotic genes, thereby creating a tumor‐supportive microenvironment [17]. This evidence concerns the gene NFKB1 and neoplasm.