Molecularly, human CHD is generally induced by two directions of abnormalities: (1) heart development: genes like NKX2-5 and GATA4 and pathways like Wnt, Notch, and BMP participate in human CHD pathogenesis by disrupting human heart development [8,9]; (2) heart structural abnormalities: fibrillin dysfunction leads to abnormal protein production, affecting the heart’s scaffolding and structural integrity [10], which further initiates CHD. Here, NKX2-5 is linked to coronary artery disorder.