Excessive abundance of IL6 also exacerbates colitis by suppressing apoptosis of infiltrating T-cells through "trans-signaling", whereby shedding of the extracellular domain from IL6Rα-proficient epithelium provides a soluble, ligand-binding receptor subunit for IL6 to activate gp130 in IL6Rα-deficient T-cells [89]. The gene discussed is IL6; the disease is colitis.