The key molecular players involved in the progression of ECD and EAS include platelet endothelial cell adhesion molecule-1 (PECAM-1), VE-cadherin, VEGFRs, MAPK/ERK, signal transducer and activator of transcription-3 (STAT-3), nuclear factor kappa B (NF-κB), PI3K/AKT, eNOS, KLF-4, and KLF-2 (Morris et al., 2020). This evidence concerns the gene STAT3 and familial atrioventricular septal defect.