This is currently less compelling for T-ALL where identification of founding lesions driving T-ALL subtypes are of biological and mechanistic interest but are not typically used to risk stratify or guide therapy, exceptions possibly being kinase inhibition for JAK-STAT alterations and ABL1 rearrangements, identification of alterations in Ras, PTEN, NOTCH1 and/or FBXW7 that have been found to be associated with outcome in some studies [188], and LCK dependence for dasatinib therapy [149]. The gene discussed is SOAT1; the disease is acute lymphoblastic leukemia.