The potential pathogenesis of lymphoproliferative diseases associated with SLE has not been established; however, the following pathogenic mechanisms have been proposed22: B‐cell hyperactivity and defective immune surveillance may help B‐cell clones escape the immune system; increased resistance to cell apoptosis may further promote the malignant transformation of tumors; and mutations in the phosphatase and tensin homolog (PTEN) gene and Bcl‐2 overexpression may be the basis for resistance to cell apoptosis. This evidence concerns the gene BCL2 and systemic lupus erythematosus.