Interestingly, in B6.Sle1b mice, STAT1 tyrosine 701 phosphorylation (STAT1-pS727) promoted germinal center (GC) responses, which drove the development of systemic lupus erythematosus (SLE), whereas STAT1-pS727 was not required for the response of GCs, Tfh cells, and antibodies to foreign antigens, suggesting that gut microbes may influence the development of autoimmune responses through different mechanisms to influence the onset and development of autoimmune responses (Chodisetti et al. 2020). The gene discussed is STAT1; the disease is systemic lupus erythematosus.