In sepsis-induced lung injury, extracellular matrix proteins are abnormally activated, accelerating their binding to the integrin receptor αvβ3, thereby recruiting and phosphorylating focal adhesion kinase (FAK), activating downstream Src family kinases, and forming the FAK/Src signaling complex (Liu Y. S. et al., 2024; Lechertier and Hodivala-Dilke, 2012), Ultimately, it leads to an increase in endothelial permeability and disrupts the integrity of the endothelial barrier. The gene discussed is SRC; the disease is Sepsis.