As a background, PTEN protein is downmodulated in 15–25% of T-ALL patients due to genetic mutations, resulting in an upregulation of the PI3K-AKT-mTOR pathway (phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin), which provides a survival stimulus for leukemic cells and, for this reason, PI3K inhibitors have started to be used in the clinical management of T-ALL. Here, PTK2B is linked to acute lymphoblastic leukemia.