Human tumor growth depends on rapidly dividing cancer cells driving population expansion. Even advanced tumors， however， contain slowly proliferating cancer cells for reasons that remain unclear. Here， we selectively disrupt the ability of rapidly proliferating cancer cells to spawn AKT1 daughter cells that are rare， slowly proliferating， tumor-initiating， and chemotherapy-resistant， using β1-integrin activation and the AKT1-E17K-mutant oncoprotein as experimental tools Surprisingly， we find that selective depletion of AKT1 slow proliferators actually reduces the growth of a molecularly diverse panel of human cancer cell xenograft models without globally altering cell proliferation or survival Moreover， we find that unusual cancer patients with AKT1-E17K-mutant solid tumors also fail to produce AKT1 quiescent cancer cells and that this correlates with significantly prolonged survival after adjuvant treatment compared with other patients. These findings support a model whereby human solid tumor growth depends on not only rapidly proliferating cancer cells but also on the continuous production of AKT1 slow proliferators. .