To determine if the upstream FEL1-4 enhancers contribute to pathogenesis of ACDMPV, we examined the multiome (snRNA + snATAC) datasets derived from lungs of two ACDMPV patients with non-coding FOXF1 deletion (designated as P1 and P2, respectively)34. This evidence concerns the gene FOXF1 and alveolar capillary dysplasia with misalignment of pulmonary veins.