Given published data showing an indispensable role of IFN-γ–STAT1–Tbet signaling in the development of autoimmune AFC and GC responses and autoimmunity in SLE-prone mice (4, 24, 25, 42) and regulation of STAT1 in B cells by the STAT4 risk allele of rs11889341 (48), it is tempting to speculate whether STAT1, and not STAT4, is the culprit gene in promoting SLE autoimmunity in patients. The gene discussed is TBX21; the disease is systemic lupus erythematosus.