Furthermore, we revealed that the progression of JAK3M511I-induced T-ALL from low to high malignancy is triggered by the coexistence of PHF6 mutation, and that provided a potential therapeutic window for the modulation of P53 and JAK3 activity in the treatment of T-ALL patients with PHF6 and JAK3 comutation. The gene discussed is JAK3; the disease is acute lymphoblastic leukemia.