Because Fe2+ and lipid ROS are essential for ferroptosis process, and malondialdehyde (MDA) is an important end product of lipid ROS [27], we further measured their concentrations in erastin- and RSL3-treated HCC cells and found that knockdown of NEAT1 significantly inhibited the accumulation of MDA, lipid ROS and Fe2+ (Fig. 2d, e, f). This evidence concerns the gene NEAT1 and hepatocellular carcinoma.