The complex involvement of abnormal diverse immune-cell subsets in SLE pathogenesis is a major contributor to the increased difficulty in treating SLE.5 6 We previously reported that the CXC chemokine receptor (CXCR) 5+CXCR3+ B cell lymphoma (Bcl) 6+T-bet+ interleukin (IL)−21+ IFN-γ+ T (T follicular helper (Tfh)/T helper (Th) 1) cells modulate the differentiation of autoantibody-producing B cells via IL-21/IFN-γ production, and their expression is increased in the peripheral blood of patients with SLE.7 This evidence concerns the gene BCL6 and systemic lupus erythematosus.