Previous work has shown that deletion of PTEN in mouse prostate drives class I PI3K-dependent epithelial cell hyperplasia and tumor growth with 100% penetrance (Jia et al., 2008, Trotman et al., 2003), and, thus, our results represent a stunning example of how deletion of PTEN in vivo can result in massive PI(3,4)P2 accumulation in the context of class I PI3K pathway activation. The gene discussed is PTEN; the disease is neoplasm.