In our murine studies, diabetes-induced retinal endpoints were further worsened in the ACE2-/y diabetic mice and maintenance of enteral ACE2 either by engineered probiotics similar to what was used in this study or by genetic overexpression of ACE2 in the gut epithelium of murine models, protected the gut barrier from the adverse consequences of diabetes [12]. The gene discussed is ACE2; the disease is diabetes mellitus.