Insertion of transposed elements within mammalian genes is thought to be an 
important contributor to mammalian evolution and speciation. Insertion of 
transposed elements into introns can lead to their activation as alternatively 
spliced cassette exons, an event called exonization. Elucidation of the 
evolutionary constraints that have shaped fixation of transposed elements within 
human and mouse protein coding genes and subsequent exonization is important for 
understanding of how the exonization process has affected transcriptome and 
proteome complexities. Here we show that exonization of transposed elements is 
biased towards the beginning of the coding sequence in both human and mouse 
genes. Analysis of single nucleotide polymorphisms (SNPs) revealed that 
exonization of transposed elements can be population-specific, implying that 
exonizations may enhance divergence and lead to speciation. SNP density analysis 
revealed differences between Alu and other transposed elements. Finally, we 
identified cases of primate-specific Alu elements that depend on RNA editing for 
their exonization. These results shed light on TE fixation and the exonization 
process within human and mouse genes.