Notably, CCL20 is known to be secreted by the biliary epithelium in response to pathogens and has been implicated as a trigger of the chronic Th17 response in a patient with primary sclerosing cholangitis (PSC) and in PSC experimental models.44,45 On the contrary, EMB organoids exposed to the same bacteria lack a response by not showing secretion of inflammatory mediators. The gene discussed is CCL20; the disease is sclerosing cholangitis.