In Nrf2-deficient B6/lpr mice, which are susceptible to LN, Th17 cell activation and STAT3 phosphorylation were increased, while the Th17 differentiation inhibitor SOCS3 (suppressor of cytokine signal 3) was decreased, indicating a protective role of Nrf2 in LN [233]. Here, STAT3 is linked to lobular neoplasia.