As we detected significantly higher IFN levels in the plasma of leukemic mice (Fig. 5E) and IFN-inducible genes in colonies, particularly in the absence of STAT3β (Supplementary Fig. 6A), we hypothesized that IFN signaling might contribute to the leukemogenic potential of AML blasts. The gene discussed is IFNA1; the disease is acute myeloid leukemia.