These findings indicate that abnormal expression of NS, in addition to causing oncogenic effects under certain circumstances and inducing p53 as an counteraction, could also stabilize tumor-suppressor ARF by enhancing the binding of NPM to ARF in the nucleolus and/or by directly interacting with ARF in the nucleoplasm when NPM is absent, providing an alternative surveillance to prevent aberrantly expressed NS-mediated tumor cell proliferation and transformation (Fig. 1). This evidence concerns the gene CDKN2A and neoplasm.