Furthermore, we demonstrated a re-induction of ISGs in BCR-ABL-positive cells after imatinib treatment and a further increase when cells were treated with a combination of TKI and IFNa (Fig. 2), most likely due to positive feedback of re-induced STAT1, loss of negatively regulating histone marks, and rescue of IFNAR1 surface expression after pretreatment of CML cell lines with TKI [26]. The gene discussed is STAT1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.