TTNF-α-induced protein 3 (TNFAIP3) can inhibit inflammatory responses by negatively regulating the NF-κB inflammatory signaling pathway; however, the transcriptional activity marker trimethylated lysine 4 of histone H3 (H3K4me3) has been shown to be reduced in the TNFAIP3 gene promoter of CD4+ T-cells in patients with SLE, resulting in a significant decrease in the TNFAIP3 mRNA level and overexpression of IFN-γ and IL-17, thereby exacerbating the inflammatory response and promoting SLE pathogenesis (128). The gene discussed is IL17A; the disease is systemic lupus erythematosus.