The frequent amplification and gain-of-function mutations of PIK3CA which encodes PI3K catalytic subunit p110a, the dysregulation of PI3K/Akt pathway due to the upstream receptor tyrosine kinase (RTK), and the loss-of-function mutations of PTEN (phosphatase and tensin homolog deleted on chromosome 10), in cancer, suggest that PI3K is a desired target for cancer therapy [4]. The gene discussed is AKT1; the disease is cancer.