More recently, acute ethanol consumption was demonstrated to worsen sepsis-induced lung injury in mice by activating the sphingosine kinase 1 (SphK1)/sphingosine-1-phosphate (S1P)/S1P receptor 1 (S1PR1) signaling pathway.127 Specifically, acute ethanol exposure led to increased pulmonary vascular permeability, neutrophil infiltration, inflammation, oxidative stress, and cell apoptosis. This evidence concerns the gene SPHK1 and Sepsis.