Secondary, although CDDP has been demonstrated to induce cancer cells into senescence through sequential activation of the DNA damage response and the p53/p21 pathway in the literature [20, 35], and in our hands, knockdown of PRMT5 was found to further promote CDDP-induced p21 expression and senescent OS cells, while PRMT5 overexpression remarkably diminished CDDP-induced p21 protein level and senescent cells. The gene discussed is CDKN1A; the disease is cancer.