The hypothesis that invadopodia p-ezrin overexpression influences their activity in breast cancer cells, at least in part, through the regulation of the NHE1 is further supported by the similar regulatory pattern of invadopodia ECM proteolysis with NHE1 mutants that cannot bind either ezrin or PIP2 (Figure 6B) as was observed above with the ezrin mutants. This evidence concerns the gene SLC9A1 and breast carcinoma.