We next investigated how loss of Fgfr2 impacts proliferation during AF closure using 5-ethynyl-2-deoxyuridine (EdU) pulse-chase experiments, since persistence of the AF in Wnt1-Cre;Fgfr2−/− mice could be due to increased proliferation in the AF and/or decreased proliferation in the osteogenic fronts of the frontal bone. This evidence concerns the gene FGFR2 and atrial fibrillation.