The fact that rabaptin-5 phosphorylation negatively affects invasion in this context and that loss of PKD1 promotes invasion while loss of PKD3 blocks invasion supports the idea that PKD1/PKD2 and PKD2/3 heterodimers have different substrate portfolios in breast cancer cells, possibly based on their different localization, and thus have opposing functions. This evidence concerns the gene PKD2 and breast cancer.