Loss of function of Brg1/Smarca4 and Baf60c/Smarcd3 in mouse embryos results in a wide range of congenital heart defects and the cardiac defects caused by Brg1/Smarca4 haploinsufficiency are exacerbated in an Nkx2.5, Tbx20, or Tbx5 heterozygous background, highlighting the genetic interaction between the BAF complex and the central members of the cardiac transcription program [55,60,63]. Here, SMARCD3 is linked to congenital heart disease.