One of these is by reversing microbial dysbiosis [46]; secondly, by inhibiting the activity of Pin-1, which activates the TLR-7/TLR-9/IRAK-1/IRF-7 signal that contributes to SLE phenotype [47]; and, thirdly, by reestablishing the vitamin A levels in SLE patients, which improves the T helper 17 (Th17) and regulatory T cell (Treg) balance [44]. The gene discussed is IRF7; the disease is systemic lupus erythematosus.