To assess the oncogenic potential of the PRL-2·CNNM3 complex, we first investigated the role of the CNNM3 D426A mutant, which has lost its ability to interact with PRL-2, in cellular proliferation by establishing cell lines stably expressing an empty control vector (pLenti6/v5), CNNM3 WT, or CNNM3 D426A in mouse DB-7 tumor-derived cell lines known to form tumors when injected into murine mammary fat pads (3, 29). The gene discussed is CNNM3; the disease is neoplasm.