Kp1B/B mice had been developed to probe the role of enhanced expression of NRF2 signaling in tissue-specific manners in the lung on cigarette smoke-induced oxidative stress and inflammation [13], and subsequently in T-cells, myeloid cells, and dendritic cells in autoimmune inflammation [28], myeloid leukocytes in sepsis [29], and kidney epithelium in hydronephrosis [30]. The gene discussed is NFE2L2; the disease is Sepsis.