Studies in acute myeloid leukemia (AML) models suggest that monocytes reprogrammed with lentiviral vectors to co-express GM-CSF, IFNα2 and antigens differentiate into induced DCs that potently activate anti-tumor T and B cells, providing a potential new therapeutic approach to address minimal residual disease following chemotherapy for AML patients [55]. The gene discussed is IFNA2; the disease is neoplasm.