AKT can be activated in cells by reduced levels or mutations in Phosphatase and Tensin homology protein (PTEN) and increased activity through mutations of the subunits of Phosphatidylinositide 3-kinases (PI3 kinases) and it has recently been reported that loss of stromal PTEN dramatically increases mammary tumour formation in a MMTV-ErbB2 breast cancer model in mice [6, 7]. This evidence concerns the gene AKT1 and breast cancer.