The DDK syndrome is known as the polar-lethal embryonic death that occurs at the morula-blastocyst stage when female mice of the DDK strain are mated with males from many other inbred strains (alien males). Embryonic death is interpreted to be caused by incompatibility between a DDK oocyte factor and the product from male pronucleus, both of which map to the Om locus on mouse chromosome 11. We compared development of DDK ×DDK embryos (high viability) and DDK × BALB/c embryos (low viability) before the morula stage (as 2 cell, 4 cell and 8 cell), there was no any morphological manifestations of DDK syndrome are observed. To make sure if the transcripts that are differentially in the DDK ×BALB/c embryos, we selected a series reference genes such as proto-oncogenes, growth factors, and growth and apoptosis genes and confirmed by quantitative RT-PCR that numbers of genes in those stages are down regulated in the DDK ×BALB/c embryos. However, except the LIF (leukemia inhibitory factor) was negative expressed and the other genes all detected in three stages. The expression of EGF (epidermal growth factor), EGF-R (epidermal growth factor receptor), Bcl-2 were significant variations (P< 0.01) at the early 4 cell and 8 cell stage, and also the test was significant variations (P<0.01) for the Mcl-1 at all the three stages. Our results indicate that the Om was effected the low-expression of functional genes indirectly to induce embryos destined to die of DDK syndrome and that the embryonic death observed is result of the regulation of multiple genes. Keywords-mouse eimplantation embry; polar-lethal embryonic death; ovum mutant or Om; DDK syndrome I.978-1-4244-9171-1/11/$26.00 ©2011 IEEE