Since JAK3 mutations could act as “driver” mutations in leukemia patients, we investigated whether PHF6 mutations act as subsequent events to promote JAK3M511I-induced leukemia development by generating Mx1-Cre;Phf6fl/y (MC Phf6fl/y) and Mx1-Cre;Phf6+/y (MC) mice, and constructed MC Phf6fl/y + JAK3M511I and MC + JAK3M511I mice (Fig. 3A). Here, JAK3 is linked to leukemia.