Previous studies have demonstrated that excessive ROS can mediate the disruption of cellular AJs.36, 37, 38, 41 For example, exposure to epidermal growth factor increased the production of hydrogen peroxide in human ovarian cancer cells, which down‐regulated E‐cadherin expression through p38 activation.41 Here, p38 inhibitor treatment reversed the effects of CXCL16 on the epithelial barrier integrity and E‐cadherin expression. The gene discussed is CXCL16; the disease is ovarian carcinoma.