Considering our previous data that Peli1 negatively regulates T cell proliferation and activation by targeting c-Rel ubiquitination28, it is reasonable to assume that Peli1 may also function in T cells to mediate the autoimmune inflammation during SLE pathogenesis, and explains the observed phenotype that the difference of lupus-like disease between WT and Peli1 global KO mice is more obvious than that in Rag1-deficient mice transferred with WT T plus WT or KO B cells. The gene discussed is RAG1; the disease is systemic lupus erythematosus.