From the results of the proteome analysis, PB application caused significant CAR- and PXR-dependent induction of phase I and II metabolic enzymes in both Ogg1 homozygous mutant and wild-type mice, but insufficient, or no Nrf2 activation in the Ogg1−/− livers and HCCs, respectively, pointing out that nonrepaired 8-OHdG and uncontrolled accumulation and damage from the reactive oxygen species in Ogg1−/− liver tissue could become the reason of progression of hepatic adenoma to carcinoma (Figure 5()). The gene discussed is NR1I2; the disease is carcinoma.