Alterations of three Akt isoforms, including amplification of Akt1, somatic (activating) mutations of Akt1,amplification of Akt2, overexpression of Akt2 without evidence of Akt2 amplification, overexpression of Akt3 mRNA and protein but lack evidence of Akt3 amplification, and somatic (activating) mutations of Akt3 have been reported in a wide range of tumour types[41-46]. The gene discussed is AKT3; the disease is neoplasm.