Δ133p53α promotes the repair of DNA double-strand breaks due to the increased expression and recruitment of RAD51, which is a DNA repair factor essential for effective homologous recombination, through the repression of full-length p53 and upregulation of E2F1, a transcription activator of RAD51. Therefore, the restoration of Δ133p53α expression may be a novel therapeutic strategy for treating ageing-associated phenotypes of HGPS in vivo [115] (Figure 4). This evidence concerns the gene RAD51 and Hutchinson-Gilford progeria syndrome.