We also speculate that intense inflammatory responses regulated by high levels of Th1 (IFN-γ and GM-CSF) and Th17 cytokines (IL-17F and IL-21) along with decreased levels of Th2 cytokine (IL-5) and free radicals (LPO and CAT) contribute to the development of LN in SLE. The gene discussed is IL5; the disease is lobular neoplasia.