The interaction between ARF and NPM can preserve ARF function by preventing its degradation, while overexpressed NPM or cancer-associated NPM mutants have been shown to inhibit ARF functions by restricting its ability to translocate between nucleolus and cytoplasm (Bertwistle et al., 2004; Kuo et al., 2004; Korgaonkar et al., 2005; Colombo et al., 2006; Moulin et al., 2008). The gene discussed is CDKN2A; the disease is cancer.