To test the hypothesis that this variation might be controlled by an environmental factor such as ID, we crossed male C57BL/6 J background mice heterozygous for either a Tbx1 null allele80 (a model of 22q11.2 deletion syndrome), or the Dp1Tyb duplication81 (a model of DS), with ID females and analysed embryonic phenotypes at E15.5. Here, TBX1 is linked to 22q11.2 deletion syndrome.