Studies from our laboratory and others revealed that P-Rex1 is an essential mediator of Rac signaling activation in response to stimulation of tyrosine-kinase receptors and GPCRs in breast cancer cells, and that it integrates signals emanating from these receptors via PIP3 and Gβγ subunits, respectively [18, 19]. This evidence concerns the gene AKT1 and breast carcinoma.