These data clearly showed that abnormally expressed miRNAs in SLE patients had a critical functional link with the aberrant DNA hypomethylation in lupus CD4+ T cells, resulting in the overexpression of autoimmune-associated methylation-sensitive genes, such as those that encode CD70 (tumor necrosis factor (ligand) superfamily, member 7 [TNFSF7]), CD40 ligand (TNFSF5), and lymphocyte function-associated antigen 1 (LAF-1, integrin αLβ2, CD11a/CD18) (54), which contributed to the autoreactivity and overstimulation of CD4+ T cells in SLE (51). This evidence concerns the gene CD40LG and systemic lupus erythematosus.