Based on bioinformatics analysis and rat model experiments, CHEN et al. found that knockdown of TLR4 or NADPH oxidase-4 (NOX4) during the development of heart failure could lead to increased expression of GPX4 and FTH1, reduced intracellular unstable iron, decreased lipid peroxidation, inhibition of left ventricular remodeling, and improvement of ventricular function; meanwhile, they also verified that TLR4 is the upstream molecule of NOX4, and proved that the TLR4-NOX4 pathway is one of the pathways related to ferroptosis in the process of heart failure [136]. Here, GPX4 is linked to heart failure.