SPI1 and systemic lupus erythematosus: The transcription regulator Bach2 is another potential target for SLE therapy, and Bach2 overexpression significantly inhibited the levels of PU.1, IRF4, IL-9, and Th9 in CD4+ T cells from SLE patients (31), implying that elevated IL-9 and Th9 levels may trigger the inflammatory process in SLE.