Pediatric T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy derived from T-cell precursors and represents 10% to15% of childhood acute lymphoblastic leukemia, the most common cancer inchildren.
In T-ALL many recurrent molecular lesions, for example, alter-ations affecting NOTCH1, PI3K/PTEN/AKT/mTOR, or JAK-STAT signal-ing pathways, hold promise for genetic-based risk stratification andtargeted therapy. Yet, the prognostic value of these alterations is still anarea of active debate and probably depends on the treatment context.For instance, PTEN abnormalities, the negative regulator of the PI3K/AKTpathway, were associated with unfavorable long-term outcome in somepediatric and adult T-ALL series,1–3 yet not all.4