To unravel a potential mechanism responsible for the observed differences in disease development and progression of NASH in mice lacking c-Met in Kupffer cells, we next investigated the amount of apoptotic cell death and the intrahepatic oxidative stress environment by TUNEL and DHE (dihydroethidium (hydroethidine)) staining (Figure 2(c), Supplementary Figures 3A and 3B). This evidence concerns the gene MET and metabolic dysfunction-associated steatohepatitis.