Consistent with our findings, several studies have demonstrated that multiple PTEN-deficient tumor types are reliant on p110β activity, with p110β–selective inhibition or genetic deletion of PIK3CB—but not PIK3CA (p110α)—sufficient to perturb PI3K/AKT signaling and abrogate tumor cell growth in vitro and in vivo, with combination therapies showing the highest potency (33, 47, 50, 51). This evidence concerns the gene AKT1 and neoplasm.