Deletion of the miR‐17‐92 cluster brought about decrease in numbers in Tfh and germinal centre of B cells, while transgenic expression of this miRNA cluster in CD4+ T cells caused increased numbers of both Tfh and germinal centre B cells.14, 15 Decreased expression of pro‐apoptotic molecule and phosphatase and tensin homologue on chromosome 10 in mice transgenic for the miR‐17‐92 cluster, lead to lymphoproliferation and other lupus manifestations.16 It is generally recognized that these cells play primary mediators in SLE. This evidence concerns the gene CD4 and systemic lupus erythematosus.