Results of studies performed in a murine model of IBD suggest that in T cell receptor α chain–deficient (TCRα-/-) mice, treatment with anti–IL-4 Ab resulted in a decrease of Th2 cytokines, and a concomitant increase of IFN-γ, suggesting that not only NK-T cells, but also CD4+ Th2 T cells play a major immunopathological role in the induction of IBD [40]. The gene discussed is IFNG; the disease is inflammatory bowel disease.