To test this hypothesis, we treated the Pten null prostate cancer and T-ALL models with 6-AN and observed significantly increased the Phlda3 mRNA and protein levels, accompanied by substantial decreases in the levels of P-AKT and P-S6 as well as the PPP metabolic intermediates (except for 6PG since 6-AN blocks the first two steps of the PPP) (Fig. 7a–c). The gene discussed is AKT1; the disease is prostate carcinoma.