With the development of molecular embryology and the coming of the post-genomic era, the molecular mechanisms of morphological evolution have recently begun to be elucidated. Whole genome sequences of many vertebrate species have been determined, and comparative genomics has suggested that one source of biodiversity is conserved non-coding elements (CNEs), which may be involved in generating new networks of gene expression. Nishihara et al. (Genome Res. 2006; 16, 864) discovered retroposon (AmnSINE1s)-derived CNEs in the human genome, and suggested that the AmnSINE1s obtained their function (i.e., exapted) in a common mammalian ancestor and are involved in generating mammalian-specific morphology. Therefore, investigation of the function of AmnSINE1-derived CNEs in morphogenesis helps us understand the molecular events of how mammals obtained their specific morphological characters by exaptation that occurred when the first mammalian ancestor emerged about 250 Ma (million years ago). Because there are more than 100 AmnSINE1-derived CNE loci in the mammalian genome, a burst of exaptation of AmnSINE1s must have occurred, possibly triggered by the Permian-Triassic mass extinction 250 Ma. In this review, we discuss morphological evolution of the mammalian-specific characters including brain that were exapted after retrotransposition of AmnSINE1s by referring to two CNE loci described by Sasaki et al.