Intriguingly, in addition to causing ACDMPV, larger-sized CNV deletions involving FOXF1 and its nearby genes FENDRR, FOXC2, and FOXL1, but not the pathogenic SNVs involving FOXF1 or deletions of its distant lung-specific enhancer only, have been also associated with severe heart defects, including hypoplastic left heart syndrome (HLHS) and single umbilical artery (SUA) [2]. Here, FOXF1 is linked to hypoplastic left heart syndrome.