PFKFB4 and acute respiratory distress syndrome: 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.