We have previously described a novel signal transduction module in breast cancer cells localized to the dominant leading edge pseudopodia that, during hypoxia or serum deprivation, increases invasive ability in human breast cancer cells by a stimulation of the NHE1 via the NHERF1 directed and PKA-mediated phosphorylation of RhoA at serine 188 and the subsequent inhibition of RhoA and p38 activities [82,83]. The gene discussed is NHERF1; the disease is breast carcinoma.