We demonstrate a potentially novel mechanism, in which miR-21 overexpression enhances Fe2+-dependent TET enzyme activity through repression of BDH2 and promotes BCL6 promoter hydroxymethylation and transcription activation, leading to excessive Tfh cell differentiation in SLE; this mechanism provides potentially novel strategies for SLE therapy (Figure 10). This evidence concerns the gene BDH2 and systemic lupus erythematosus.