How the uterus evolves to allow a blastula to implant is a topic of intense scientific interest. Recent results show that, in mice, the developmental gene HoxA10 plays an important role in regulating uterine receptivity. The HoxA10 protein regulates the development of the uterus in the embryo of many species, but in mice, HoxA10 evolved a secondary role of regulating the development of dome shaped extensions of uterine epithelia called uterodomes. Uterodomes are necessary for uterine receptivity to implantation in the mouse. The presence of HoxA10 in the adult uterus does not guarantee the expression of uterodomes, however, as HoxA10 protein has been found by Western blot in the oviparous lizard Lampropholis guichenoti that does not display uterodomes as well as the viviparous lizard Eulamprus tympanum that does display uterodomes. Studies using antisense oligonucleotides that bind and inhibit the start of translation site of HoxA10 demonstrate that down-regulating HoxA10 production inhibits uterodome formation and implantation in mice. Similar antisense technology could be used in viviparous lizards to determine whether HoxA10 is regulating uterine receptivity in various species. The first stage in such a strategy would entail sequencing the region of lizard HoxA10 that contains the start of translation site. Once this sequence is known for a particular species, antisense oligonucleotides can be designed to inhibit HoxA10 and the effects of this on uterine receptivity can be studied. If several species of lizard that evolved viviparity independently are all shown to rely on HoxA10 to regulate uterodome development and uterine receptivity it will indicate that HoxA10 is a vital part of the evolution of viviparity. It will be interesting in future studies to determine which cells of the lizard uterus express HoxA10 and whether, like the mouse, the expression of lizard HoxA10 is regulated by co-factors such as vitamin D.