If this hypothesis holds true, these mutations would lead to upregulation of Th17 cells in parallel to the inhibition of Tregs; this could translate into an increased production of IL-17 and IL-22 that might contribute to the greater rate of autoimmunity and cytopenias reported here for STAT3-mutated vs. WT LGLL patients. The gene discussed is IL22; the disease is T-cell large granular lymphocyte leukemia.