These data demonstrate that a single copy of myr-p110α does not saturate the PI3K signaling pathway with regard to p-AKT levels and two copies of myr-p110α further activate PI3K signaling to a greater degree than that induced by a single copy of myr-p110α in mammary tumors, resulting in the increased rate of tumor initiation. The gene discussed is AKT1; the disease is breast cancer.