An earlier study with ITK-/- donor T cells in an allo-HSCT mouse model has already reported comparable beneficial effects on GVHD and observed reduced expression of IRF4, JAK1, JAK2, and STAT3 as well as phosphorylated forms of JAK1, JAK2 and STAT3 if ITK was absent in T cells, which might explain impaired differentiation capacities observed in the ITK inhibitor study (226). The gene discussed is JAK1; the disease is graft versus host disease.