Bornschein and coworkers [53] took advantage of a recently-developed murine pro-T-cell culture system [54] for unraveling the mechanisms underlying the cooperation between TAL1 transcription factor overexpression and Pten deletion, i.e., a combination of abnormalities frequently observed in T-ALL patients (see further on in this review) [55,56]. This evidence concerns the gene TAL1 and acute lymphoblastic leukemia.