In summary, integrated analyses of genomic DNA and RNAseq in CHD cardiac tissues identified preferential silencing of paternally expressed imprinted genes, several extreme ASE and LOE genes relevant to cardiogenesis and potential downstream targets of KMT2D. DNA sequence analyses of 81 trios identified nine de novo mutations likely responsible for disease4, 8. The gene discussed is KMT2D; the disease is coronary artery disorder.