Even in the absence of such mutations, it has been observed that the PI3K/AKT pathway is constitutively activated in the majority of pancreatic cancers, through aberrant expression of PTEN as well as amplification or activation of AKT2 kinase (Cheng et al., 1996; Ruggeri et al., 1998; Schlieman et al., 2003; Asano et al., 2004; Reichert et al., 2007; Koorstra et al., 2008). This evidence concerns the gene AKT1 and pancreatic neoplasm.