It has been also reported that HDAC3 physically interacts with RUNX2 thus suppressing its transcriptional activity [81] Furthermore, dysregulation of HDAC3 mediated epigenetic silencing of TGFβ1 (transforming growth factor beta 1) is required during valve development to maintain VICs quiescence and may represent a predisposing factor for development of BAV and other congenital heart diseases [82]. Here, HDAC3 is linked to congenital heart disease.