CCL5 and hepatocellular carcinoma: [25] confirmed that CCL5 from CAFs can inhibit ubiquitination and degradation of hypoxia‐inducible factor 1 alpha (HIF1α) by binding to specific receptors, thereby maintaining HIF1α under normal oxygen conditions, upregulating the downstream gene zinc finger enhancer‐binding protein 1 (ZEB1), and inducing EMT, which ultimately promotes the lung metastatic ability of HCC cells.