Hence, we sought to selectively assess the contribution of GM-CSF to the manifestation of RORγt-independent intestinal GvHD by treating RORγt-deficient donor T cell receiving mice either with an IL-7R blocking antibody over the first half of the observation period together and anti-GM-CSF antibody throughout the experiment or with an isotype control antibody alone as described before (17). The gene discussed is IL7R; the disease is graft versus host disease.