Inhibition of ferroptosis has been demonstrated to markedly mitigate sepsis-induced ALI, highlighting the complexity of the mechanisms initiating ferroptosis, including the dysregulation of the cystine/glutamate antiporter system (System Xc−), composed of the SLC7A11 and SLC3A2 subunits, is essential for intracellular free radical scavenging and GSH production, with its inhibition leading to decreased cellular GSH levels and increased ROS production [43]. The gene discussed is SLC3A2; the disease is Sepsis.