For this difference between the genotypes of the rest of the embryo in the two experimental approaches to explain the results, a critical determinant of ASD risk would have to lie in some lineage other than those represented by cTnt and Sox17. Furthermore, in that lineage, risk would have to be conferred by being Nipbl–wildtype, while protection would have to be conferred by being Nipbl-deficient. This evidence concerns the gene TNNT2 and atrial septal defect.