Since we did not observe any cardiac abnormalities in the mice with genotype of 129-IIA−/− in embryonic or postnatal stages (Supplemental Table 1), and assuming that the ES cell used for generating the IIA-null mutant was indeed a hybrid of 129S1/SvImJ and 129X1/SvJ, we hypothesized that this segment of DNA contained a mutation that caused CHD, which was generated during the targeted disruption of Col2a1 and cosegregated with the IIA-null locus. This evidence concerns the gene COL2A1 and coronary artery disorder.