In the current study, we further demonstrate and confirm that the pharmacologic inhibition of JAK1/JAK2 preserves the beneficial anti-leukemia effect previously reported by our group in IFNγR−/− T cells [3] in two different leukemia models (A20 lymphoid leukemia and APL myeloid leukemia). Here, IFNGR1 is linked to acute promyelocytic leukemia.