Given that all of the Xenopus, murine and human SOXF factors have a conserved β-catenin binding domain at the C-terminus and interact with β-catenin to repress the activity of β-catenin/TCF transcriptional complexes, and therefore suppress the Wnt/β-catenin signaling [86], the SOX18 mutation identified in our study contributed to PDA probably by a similar mechanism. This evidence concerns the gene HNF4A and Patent ductus arteriosus.