It was previously found that in mice, the conditional loss of the BAF subunit ARID1A (AT-rich interactive domain-containing protein 1A), a known tumor suppressor, led to altered cardiac NC migration, improper NC colonization to the OFT, and impaired conotruncal septation (Figure 1), potentially due to ARID1A-contain BAF complexes being the predominant form of the SWI/SNF complex in cardiac NCCs [96]. The gene discussed is ARID1A; the disease is neoplasm.