There is considerable recent progress in using immune therapy to treat lymphoid including monoclonal antibodies, antibody-drug and -radionuclide conjugates, bi-specific antibodies and chimeric antigen receptor T-cells (CAR-T-cells). Targets of these therapies are B-cell lineage-specific antigens such as CD19, CD20 and BCMA, not cancer-specific antigens. Given these immune therapy advances in lymphoid cancers one might expect similar success using immune therapy to treat acute myeloid leukemia (AML). However, this is not so. There is only one FDA-approved therapy of myeloid cancers, gemtuzumab ozogamicin (Myelotarg®) for AML approved > 10 years ago. Why this discordance? The answer lies in two considerations: (1) lack of a robust AML-specific target antigen(s); and (2) unacceptable adverse effects resulting from non-specificity of lineage-specific antigens such as CD33 and CD124. Also, most data suggest less immune surveillance against myeloid cancers compared with lymphoid cancers. For example, AML cells have an average of 0.28 mutation per megabase of DNA compared with 8.15 mutations for lung cancer, 40-fold less. The exception is the anti-AML effect associated with haematopoietic cell transplants, so-called graft-versus-leukaemia (GvL). However, this effect occurs only in an allogeneic setting and is difficult or impossible to distinguish from graft-versus-host disease (GvHD). We can envision potential anti-AML immune therapy using two strategies: (1) antibodies; and (2) cell therapies. Synthetic biology may offer a solution to the problem of the lack of an AML-specific target antigens. I discuss the current state of immune therapy of AML and potential future directions. So, will immune therapy cure AML? Stand by.