Less commonly, it could also result from the mutational activation of Ras oncogene that activates Akt through the PI-3K pathway (Datta et al, 1996; Liu et al, 1998) or from the mutational inactivation of the PTEN tumour-suppressor gene that normally inhibits Akt activity by dephosphorylating the PI-3,4,5-P3 and PI-3,4-P2 produced by PI-3K (Stambolic et al, 1998; Ramaswamy et al, 1999). This evidence concerns the gene AKT1 and neoplasm.