Moreover, and consistent with our findings, studies by other investigators using the MRL/lpr26 and Lyn−/−39 mouse models of SLE have shown that complete deletion of MyD88 in B cells is sufficient to abrogate ANA production (but not that of total IgG), proteinuria, and glomerulonephritis, and as with ES-62, reduces the number of plasmablasts while increasing the numbers of follicular and total splenic B cells. This evidence concerns the gene MYD88 and glomerulonephritis.