PTEN and neoplasm: 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).