While the mechanistic underpinnings of this circuitry await further investigation, our work entails important translational implications: on the one hand, we suggest that octn genotyping in IBDs patients combined with microbiota profiling could help monitor the progression of the disease and predict the individual response to therapy; moreover, by reinforcing the notion that OCTN1 participates as a causative or predisposing factor to IBD, our work lays the groundwork for novel targeted therapies aimed against this carrier and/or its transported substrates. Here, SLC22A4 is linked to inflammatory bowel disease.