Further validation of this model in different patient cohorts and further basic science investigation into the molecular mechanisms of NT-proBNP and FGF23, especially in the context of AF and co-morbid heart failure or CKD, would be useful to validate this finding and to understand the drivers of AF linked to elevated FGF23 and NT-proBNP. This evidence concerns the gene FGF23 and atrial fibrillation.