An abnormal increase in intestinal permeability has been associated with CD progression, low responsiveness to therapy, and, above all, with modulation of the expression of several proteins in the colon tract involved in the water channel, such as Aquaporin (AQP) and tight junctions (e.g., TJP1 or ZO-1, Claudin1, Claudin2, Occludin) [8,9,10,11,12], also during disease flares. The gene discussed is CLDN2; the disease is Cowden disease.