Receptor tyrosine kinase-phosphatidylinositol 3-kinase (PI3K) signaling is a central integrator of metabolism, cell growth and cell survival, and deregulated PI3K signaling increases tumorigenicity.1, 2 Cancer-associated mutations occur in several components of the pathway including activating mutations of both the PI3K catalytic subunit α-isoform gene (PIK3CA, p110α)3 and the downstream signaling molecule AKT1,4 as well as deletion of the negative pathway regulator, PTEN. 5 These alterations all result in increased activity of the PI3K signaling pathway. This evidence concerns the gene PIK3CA and cancer.