Interestingly, unlike the Akt1−/− and Akt3−/− mice, in which GSK-3 activity is high and does not appear to be inhibited in response to Jenv signaling, Akt2−/− mice possess a high level of basal GSK-3α/β phosphorylation which surprisingly decreases with increased tumor burden. The gene discussed is AKT3; the disease is neoplasm.