TFF3-mediated disruption of LINGO2/EGFR complexes seems to operate similar to a rheostat tuning the extent of EGFR activity inasmuch as total LINGO2 deficiency was deleterious due to excessive basal EGFR activity, but loss of TFF3 was somewhat protective against colitis (Fig. 5d, e) and also impaired worm immunity. The gene discussed is LINGO2; the disease is colitis.