Combining the dysregulation of gene transcription involved in cardiac development, these findings suggested a potential mechanism for NKAP p.R330C‐induced CHD: the mutation alters Nkap protein intra‐nuclear distribution and inhibits its binding to Hdac3 protein, thereby disrupting the transcription of cardiac development‐related genes and ultimately leading to CHD, manifested as ventricular septal defect, overriding aorta and pulmonary stenosis (Figure 4C). This evidence concerns the gene HDAC3 and coronary artery disorder.