Similarly, significant increase in the expression of MHC-II molecules and killing of leukemia cells was found to be mediated by IFNγ secretion from CD4 T-cells in a series of in-vitro experiments testing the activity of CD123-directed immunotherapies (flotetuzumab, a CD123xCD3 dual affinity retargeting protein [DART], as well as CAR T-cells directed against CD123) both in cell lines and xenograft models from patients with relapsed AML after allo-HCT with low baseline MHC-II expression [172]. The gene discussed is IFNG; the disease is acute myeloid leukemia.