In D2→F1 chronic GVHD, D2 mice have a naturally occurring defect in initial IL-2 production that results in skewing of the initial donor CD4 T cell response away from a Th1 program, instead promoting the differentiation of T follicular helper (Tfh) cells and enhanced IgG antibody production [3, 12]. The gene discussed is IL2; the disease is chronic graft versus host disease.