In the context of cancer, the activation of this pathway occasionally may be achieved via activating mutations or the amplification of individual AKT isoforms or, more commonly, via activating mutations in the catalytic subunits of PI3K, via the loss of the tumor suppressor PTEN, or via the activation of receptor tyrosine kinases [96,103] that serve as upstream regulators of PI3K. The gene discussed is AKT1; the disease is neoplasm.