Since impaired mucus production and obesity-driven intestinal inflammation are the likely mechanisms increasing permeability of the mucosal barrier and systemic endotoxin levels33, 34 (Fig. 2), we hypothesised that in obese mice treated with IL-22, reduced ER stress and inflammation would lead to improved intestinal barrier function. The gene discussed is IL22; the disease is obesity due to melanocortin 4 receptor deficiency.