Hypodiploid B-ALL cells exhibit activation of Ras and phosphoinositide-3 kinase (PI3K)/Akt/ mechanistic target of rapamycin (mTOR) signaling pathways and are sensitive to PI3K and PI3K/mTOR inhibitors, suggesting another possible therapeutic approach for both near-haploid and low-hypodiploid B-ALL [6]. This evidence concerns the gene AKT1 and acute lymphoblastic leukemia.