Patients with detectable SETBP1 protein at diagnosis have inferior overall survival. (A) SETBP1 protein expression is significantly elevated in younger AML patients with adverse karyotype (P = .001; Mann-Whitney U test). Error bars are standard error of mean. (B) Kaplan-Meier estimates for overall survival in all patients. All AML patients are stratified into diagnostic SETBP1 terciles: absent (T1), intermediate (T2), and high (T3). (C) Young adverse patients. (D) Relapse-free survival for younger adverse AML patients, stratified by the SETBP1 level at diagnosis. The numbers of assessable cases are shown below each plot. (E) High AKT^S473 level is associated with inferior overall survival. (F) Kaplan-Meier estimates for overall survival for young adverse AML patients stratified by quartiles according to the AKT^S473 level at diagnosis. High AKT^S473 level is associated with inferior overall survival (P = .05; log-rank test). (G) Suggested model of PP2A inhibition in AML. In normal karyotype patients, PP2A is inhibited predominately by CIP2A whereas in adverse-risk patients, SETBP1 inhibition dominates. PP2A inhibition from either source results in high levels of AKT^S473. *Denotes statistical significance when compared to normal MNC cells. CR, complete remission.