Nonetheless, an interesting finding in this study is that the cardioprotective and anti-fibrotic potentials of urolithins A against STZ-induced DC are associated with upregulating the transcription and the translation, as well as increase the nuclear localization and activation of SIRT1 which resulted in subsequent deacetylation of Nrf2, FOXO1, NF-κB, and p53. The gene discussed is TP53; the disease is dyskeratosis congenita.