A clinical trial shows that estradiol concentrations were found to be significantly lower in pregnant women with SLE throughout pregnancy when compared with healthy pregnant women.[17] Antiestrogen receptor α (anti-ERα) autoantibodies that interfere with T lymphocyte homeostasis were present in 45% of the patients with SLE.[18] The lower estrogen levels and the presence of anti-ERα autoantibodies may have contributed to insufficient growth of the uterus that it can’t accommodate the rapid fetal growth, resulting in UR. The gene discussed is ESR1; the disease is systemic lupus erythematosus.