In a murine model of HF (i.e., 12-weeks post-myocardial infarction induced by permanent left anterior descending coronary artery ligation; average ejection fraction of 46.7 ± 7.5%), we observed significantly reduced pulmonary CFTR protein expression (Figure 1a), which was accompanied by an elevation of overall pulmonary S1P levels (Figure 1b). This evidence concerns the gene CFTR and hydrops fetalis.