In conclusion, our study showed that PPARγ agonists repressed the stem cell-like phenotype of HCC via NOX2-mediated oxidative stress; this effect, however, was partially attenuated by the activation of AKT, indicating a negative feedback loop between oxidative stress and AKT hyperactivation during a PPARγ agonist-mediated suppressive event (Figure 6E). The gene discussed is AKT1; the disease is hepatocellular carcinoma.