Conversely, as we also showed here, naïve mature IgM+IgD+ B cells submitted to stimuli that induced CSR to isotypes other than IgD, such as IgA (by LPS plus IL-4 and RA), further upregulated Zfp318 transcripts and Zfp318 protein, concomitant with no Sμ–σδ recombination, but rather allowing for massive expression of mIgD rather than sIgD. This evidence concerns the gene ZNF318 and rheumatoid arthritis.