Recent literature has further demonstrated that histone lactylation-regulated METTL3 promotes ferroptosis and exacerbates sepsis-associated lung injury, while pharmacological blockade of GPR81 signaling emerges as a viable strategy to disrupt lactate-induced METTL3 overexpression, thereby preserving alveolar epithelial integrity through ferroptosis inhibition and mitigating lung injury progression (28). This evidence concerns the gene METTL3 and Sepsis.