Treatment of cells with the receptor TKI ruxolitinib (and to a lesser extent IFN-γ) enhanced the expression of MHC-II on CML stem/progenitor cells and was associated with an increase in CML cell immunogenicity (enhanced CD4+ T cell proliferation) in a JAK-dependent manner (97, 98). The gene discussed is IFNG; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.