We observed that TNF‐α induced an inflammatory phenotype through NF‐kB activation, leading to increased production of pro‐tumorigenic chemokines such as CCL2, CXCL8, and CCL5.[20] Additionally, the TGF‐β signaling pathway in fibroblasts played a central role in fibroblast activation, metabolic reprogramming, and tumor‐promoting functions, contributing to the remodeling of the TME. The gene discussed is NFKB1; the disease is neoplasm.