Phosphoinositide 3-kinase (PI3K) catalyzes the production of phosphatidylinositol- 3,4,5- triphosphate by phosphorylating phosphatidylinositol (PI), phosphatidylinositol-4-phosphate (PIP), and phosphatidylinositol-4,5-bisphosphate (PIP2). Growth factors and hormones trigger this phosphorylation event, which in turn coordinates cell growth, cell cycle entry, cell migration, and cell survival (1). PTEN reverses this process, and research studies have shown that the PI3K signaling pathway is constitutively activated in human cancers that have loss of function of PTEN (2). PI3Ks are composed of a catalytic subunit (p110) and a regulatory subunit. Various isoforms of the catalytic subunit (p110a, p110b, p110gamma, and p110delta) have been isolated, and the regulatory subunits that associate with p110alpha, p110beta, and p110delta are p85a and p85b (3). In contrast, p110gamma associates with a p101 regulatory subunit that is unrelated to p85. Furthermore, p110gamma is activated by Betagamma subunits of heterotrimeric G proteins (4).