Interestingly, LGL leukaemia patients with multiple STAT3 mutations have a higher incidence of RA (43%) than patients without STAT3 mutations (6%)14, thus raising the possibility that patients with STAT3-mutated LGL leukaemia and clonal-lymphocyte proliferation are at a greater risk of developing a non-malignant autoimmune disease and that CD8+ T-cell clones carrying somatic mutations may participate in the autoimmune process. Here, CD8A is linked to autoimmune disease.