Increased expression of the proinflammatory cytokine Interleukin-6 (IL-6) in DCs of Prdm1 CKO mice, following Toll-like receptor (TLR) 4 stimulation, leads to an enhanced differentiation of follicular helper T cells (TFH), revealing a potential pathogenic mechanism for PRDM1 in autoimmune diseases (11). This evidence concerns the gene PRDM1 and autoimmune disease.