Thus, to assess the oncogenic capability of the CNNM3 D426A mutant that lost its ability to interact with PRL-2, we generated stable mouse mammary tumor DB-7 cells (3) co-overexpressing CNNM3 WT-v5 or CNNM3 D426A-v5 (Fig. 4A) and luciferase, which were injected in the mammary fat pads of athymic nude female mice. This evidence concerns the gene PTP4A2 and breast cancer.