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. The gene discussed is CD79A; the disease is rheumatoid arthritis.