Compared with the non‐IBD individuals, increased tissue expressions of Th1 cytokines (IFN‐γ and TNF‐α) could strongly suppress the BCL‐GS expression, which differentially regulated the inflammatory chemokines (CCL5 and CCL20) and thereby might drive the pathophysiology of IBD (Figure 4C).64 The gene discussed is CCL5; the disease is inflammatory bowel disease.