Based on the many substrates and dual roles of NEDD4-1, strategies for blocking the interactions between NEDD4-1 and particular substrates with the fewest side effects may be more suitable for therapeutic treatment than strategies targeting NEDD4-1 activity directly, for example, attenuating the stabilization of MDM2 by NEDD4-1 (as shown in Fig. 3a) and enhancing the degradation of N-Myc by NEDD4-1 (as shown in Fig. 3b) to inhibit cancer cell proliferation. The gene discussed is NEDD4; the disease is cancer.