Consistent with our hypothesis, we found that HIF1A drove the induction of isoform 3 of the 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3), leading to an enhanced capacity for glycolysis as an endogenous protective pathway by which excessive alveolar inflammation is counterbalanced during ARDS. This evidence concerns the gene PFKFB2 and acute respiratory distress syndrome.