DAND5 is an extracellular BMP/TGF-β/Nodal signaling antagonist essential for left-right axis establishment during embryonic development 1. As part of a conserved genetic module in vertebrates with motile cilia in their left-right organizer, DAND5 functions downstream of leftward flow and upstream of asymmetric mRNA decay, which is regulated by the RNA-binding protein Bicc1 through recognition of specific 3'UTR sequences 23. Beyond laterality determination, DAND5 independently regulates cardiac development through TGF-β/Nodal pathway modulation and exhibits anti-angiogenic activity by suppressing endothelial cell sprouting and proliferation, potentially by altering cellular redox and glycolytic balance 4. Loss-of-function DAND5 mutations cause heterotaxy with congenital heart defects in humans 1. In vitro studies using gene-edited hiPSC-derived cardiomyocytes reveal that DAND5 absence increases proliferation, upregulates cardiac progenitor markers, and impairs electrophysiological maturation, including prolonged field potential duration and reduced conduction velocity 5. These findings establish DAND5 as a critical regulator of both embryonic symmetry breaking and cardiac development, with therapeutic implications for treating congenital heart disease.