Transposable elements are mobile DNA sequences capable of self-replication within the genome, which may lead to various forms of DNA damage. The introduction encompasses the diverse classes and subclasses of TEs, particularly emphasizing the most active TEs present in the human genome. An analysis of the retrotransposition process of TEs is presented, illustrating how this mechanism can result in DNA damage and gene rearrangements. Furthermore, the review meticulously examines the implications of TE insertions on gene expression and genomic organization, which may contribute to the development of various diseases, including cancer. The relationship between TE activation and the aging process is also explored, emphasizing that epigenetic modifications associated with aging can lead to the derepression of TEs, thereby promoting genomic instability and inflammation. These factors may play a significant role in the pathogenesis of age-related diseases, such as cancer, cardiovascular disorders, and neurodegenerative conditions. Finally, the review considers potential therapeutic approaches aimed at targeting TE activity to alleviate the impacts of aging and associated diseases. Highlights 1. One of the principal mechanisms through which transposons induce DNA damage is by causing double-strand breaks (DSBs) in the DNA molecule. 2. The level of recombination has been established as being positively correlated with the abundance of TEs. 3. Additionally, transposable element insertions can also alter mRNA splicing and cause aberrant alternative splicing, leading to the skipping of exons or retention of introns. Consequently, aberrant gene expression ensues. 4. An imbalance in TE repression often occurs during aging or other processes, leading to TE activation and subsequent DNA damage. 5. TE activation-induced DNA damage contributes to aging and age-related diseases