This is consistent with the role of L1s in Z-VAD-FMK X-inactivation activity, where L1s are thought to act as boosters of X-inactivation chromosome spreading from a center of inactivation. For autosomal and X-chromosomes, intergenic L1 densities are much higher than intragenic ones. The lower density of intragenic versus intergenic L1 in both species suggests that L1 retrotransposition into genes is likely to be deleterious and would selected against in evolution. This purifying selection in the X and autosomes could be facilitated by recombination of homologous chromosomes or homologous recombination DNA break repair. Ychromosome is hemizygote and majority of the chromosome lacks homologous recombination. If the role of intergenic L1s is related to homologous recombination or homologous chromosome, intergenic L1s in Y-chromosome may have no function and can be considered as junk DNA. Rearrangements and deletion mutations of intergenic L1s in Y-chromosome should not affect fitness and the L1s should be continuously lost during evolution. In contrast to intergenic L1s, intragenic L1s possess gene regulatory function and should be conserved. As a result, in Y chromosome, intragenic L1 density is higher than intergenic for both mouse and human. Intragenic L1s are more conserved than intergenic L1 for the mouse and human. Interestingly, mouse intragenic L1s are overall less conserved than human. The lower conservation of mouse L1 is particularly marked in the 59 UTR, in which variation in monomer repeats was shown previously to control L1 promoter activity. The significantly higher mean number of monomer repeats in intragenic compared with intergenic L1s suggests that intragenic L1s are more transcriptionally active. The difference in mechanism of transcriptional control in human and mouse L1 may suggest that the transcriptionally active L1s have acquired biologically important functions independently in different mammalian lineages, i.e., convergent evolution. The greater conservation and possible activity of intragenic L1 in mouse is suggestive of function. We investigated whether intragenic L1 might play a role in gene regulation in early embryogenesis. Significant associations were found for down regulated genes with intragenic L1 and down regulation of the genes, starting from the 2-cell to the morula stage in mouse, whereas associations were significant for 8-cell to blastocyst in human. The different “L1 associated with down regulation” profiles align well with the varying zygotic activations and the levels of global hypomethylation among mammals. In particular, mouse zygotic activation starts from 2-cell division, whereas activation starts during the 4 to 8 cell divisions in human. Furthermore, mouse embryos undergo demethylation after fertilization to become hypomethylated, and establish new methylation patterns at the blastocyst stage. The mouse LaD pattern thus agrees with the global hypomethylation profile during zygotic activation. Human embryogenesis differs from mouse in the timing of zygotic activation and the human LaD pattern aligns with the slower onset of activation in human.