Together, these results indicate that Set1 regulates the expression of CREMα, and this regulation is accomplished at least partly via changing H3K4me3 enrichment at the CREMα promoter; and the up-regulated Set1 binding at the promoter augments the generation of CREMα in SLE CD4+ T cells, subsequently results in IL-2 reduction and IL-17A overproduction. Here, IL17A is linked to systemic lupus erythematosus.