The selective depletion of CD103+Vγ4 cells in IBD, linked with deficiencies in BTNL3/BTNL8 expression, and the possible reconstitution of the γδ IEL compartment upon remission reported in this paper1 paves the way for similar studies in other barrier diseases affecting, e.g., the lung or skin. The gene discussed is BTNL3; the disease is inflammatory bowel disease.