Messenger RNA (mRNA) sequences containing AU (Adenine and Uracil) rich element (ARE), are subjected to rapid degradation at their 3’ untranslated regions (UTR). The efficiency of the degradation depends on the number of AUUUA motifs. Here, we show the significant portion (30-40%) of ARE in mRNA 3’UTR was found in the short interspersed nucleotide element (SINE) at the maximum AUUUA repeats, of which function has been not known in mammalian. Alu interspersed in human genome and Alu-like sequence such as B1 or B2 in mouse have poly-adenine (poly-A) regions at the end that lead to poly-thymine (poly-T) regions at the poly-A’s complementary strand on DNA. The poly-T has ARE through the transitions from thymine to non-thymine base in regular interval. The possible transitional mechanism on how SINE’s poly-T could acquire AREs is suggested through the comparison between human mRNA’s ARE generated by Alu and orthologous chimpanzee cDNA sequence’s. In addition, all Alu sequences in chimpanzee chromosome 21 and human 22 were also aligned to search for the transition process. In this study, we suggest that SINE, which has been reported as a junk DNA element, is a source of AREs, which control mRNA life time in mammalian. The ARE was generated by the transition from thymine to adenine in SINE’s poly-T region at the 3’UTR in mammalian mRNA.