https://www.selleckchem.com/products/ml348.html Moreover, icariside I significantly upregulates CD8+T cells in both peripheral blood and tumor tissues of tumor-bearing mice. Consequently, interferon-γ (IFN-γ) secreted by CD8+T cells suppresses tumor growth through activation of JAK1-STAT1 signaling, thus inducing tumor cell apoptosis. These results suggest that icariside I could be an effective small molecule drug for tumor immunotherapy by blocking kynurenine-AhR pathway and tumor immune escape. These results suggest that icariside I could be an effective small molecule drug for tumor immunotherapy by blocking kynurenine-AhR pathway and tumor immune escape.Non-alcoholic fatty liver disease (NAFLD) is a public health problem associated with high mortality and high morbidity rates worldwide. Presently, its complex pathophysiology is still unclear, and there is no specific drug to reverse NAFLD. Ferroptosis is an iron-dependent and non-apoptotic form of cell death characterized by the iron-induced accumulation of lipid reactive oxygen species (ROS), which damage nucleic acids, proteins, and lipids; generate intracellular oxidative stress; and ultimately cause cell death. Emerging evidence indicates that ferroptosis is involved in the progression of NAFLD, although the mechanism of action of ferroptosis in NAFLD is still poorly understood. Herein, we summarize the mechanism of action of ferroptosis in certain diseases, especially in the pathogenesis of NAFLD, and discuss the potential therapeutic approaches currently used to treat NAFLD. This review also highlights further directions for the treatment and prevention of NAFLD and related diseases. The improvements of antitumor effects and tolerability on chemotherapy for advanced hepatocellular carcinoma (HCC) are warranted. Here, we aimed to elucidate the mechanism of the combining effect of tyrosine kinase inhibitor sorafenib (SOR) and iron chelator deferasirox (DFX) in human hepatoma cell lines, HepG2 and Huh-7. The