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. The gene discussed is PTEN; the disease is systemic lupus erythematosus.