The clue that NPM1 and AKT work together to promote proliferation and survival of BRAFV600E mutant colon cancer cells came from a previous study showing that either pharmacological inhibition of NPM1 function by NSC348884 at a sub-toxic concentration or NPM1 knockdown strongly potentiated anti-proliferative effects of standard chemotherapeutic agents and augmented apoptosis induction in RKO cells, which was accompanied by diminished expression levels of phospho-AKT (Ser473) [27]. The gene discussed is AKT1; the disease is colonic neoplasm.