Mechanistic studies using in vitro cell cultures and animal models have consistently shown that ETS2 regulates epithelial cell homeostasis, including proliferation, apoptosis, and differentiation.[36–40] These studies demonstrated that ETS2 modulates the expression of tight junction proteins (claudin, occludin, zonula occludens-1), which are essential for intestinal barrier integrity.[42–44] Disruption of ETS2, especially under inflammatory cytokine influence (e.g., TNF-α, IFN-γ), leads to tight junction disassembly and increased permeability,[45,46] a hallmark of IBD pathogenesis. The gene discussed is ETS2; the disease is inflammatory bowel disease.