The tumor microenvironment (TME), comprising immune cells (e.g., myeloid-derived suppressor cells, tumor-associated macrophages), stromal fibroblasts, and vascular endothelial cells, exploits this inflammatory circuitry by repurposing cytokines like IL-1β and IFN-γ to activate invasion-associated MMPs and immune-evasion pathways (Figure 4) (Eggert and Greten, 2017; Wang et al., 2024). The gene discussed is IL1B; the disease is neoplasm.