The potential role of Alu mobility in development of drug resistance in colorectal cancer cells. A typical model Alu element is approximately 300 bp in length and has a dimeric structure. The elements are composed of two similar but not-equivalent monomers (7SL-derived left monomer and 7SL-derived right monomer) joined by an A-rich linker. In the 7SL-derived left monomer, there are Box A and Box B, serving as internal Pol III promoter elements, which are helped by an up-stream Pol III enhancer for efficient transcription. The right monomer is followed by a short poly(A) tail and the both terminal sequences typically are Target Site Duplication (TSD) sequences (typically, AA\TTTT). In somatic cells, Alu elements are silent. During tumorigenesis and cancer therapy, in response to the environmental stress induced by carcinogen(s) or chemotherapeutic drug(s), the mobility of Alu elements is activated as a genomic response. Alus propagate using a ‘copy and paste’ mechanism. In the ‘copy’ phase, Alus are typically transcribed by RNA polymerase III. For the ‘paste’ phase, Alus use a ribonucleoprotein complex composed of an endonuclease and a reverse-transcriptase encoded by L1. The endonuclease initially cleaves one DNA strand, and the reverse-transcriptase copies an Alu transcript into a single strand of DNA at that genomic location. The second DNA strand is cleaved by an unknown mechanism, and then the DNA repair mechanism generates the strand complimentary to the novel Alu insertion. The process is named Target-Primed Reverse Transcription (TPRT). Because of the two distinct single-strand breaks, the final DNA sequence contains a TSD, which is a sequence of 4 ~ 25 bp repeated just before and just after the new Alu element.