BNP (B-type natriuretic peptide) and its amino-terminal cleavage equivalent (NT-proBNP) are released into the circulation from the myocardium as a result of end-diastolic wall stress, which, in turn, results from an increase in volume or pressure [10]. A recent study revealed that NT-proBNP is independently linked to the occurrence of heart failure (HF) and enhances the prediction of HF risk beyond traditional risk factors. This holds true even among individuals with obesity [10]. This evidence concerns the gene NPPB and hydrops fetalis.