Interestingly, in a mouse model for Apert syndrome, which harbors the gain-of-function variant Fgfr2S252W that causes both craniosynostosis and a persistent AF, the premature fusion of the coronal suture has been linked to activation of WNT signaling through increased expression of the Frizzled co-receptors Lrp5 and Lrp6 (Min Swe et al., 2020). This evidence concerns the gene LRP5 and atrial fibrillation.