In agreement, it has been observed that the absence of Cerl2 (DAND5 mouse homolog) in Cerl2 KO mice leads to several cardiovascular malformations, including incomplete atrial and ventricular septation, conotruncal defects, ventricular hypertrophy, and/or to laterality defects like left isomerism and thoracic heterotaxy or situs inversus [30, 31]. Here, DAND5 is linked to cardiac hypertrophy.