(A) Potential schematic for antibody-specific induction of oncosis in AML following allogeneic HSCT. Normally located within the cytoplasm and nucleus, the spliceosome complex U5 snRNP200 becomes expressed on the cell surface of AML blasts via an undefined cell stress–inducible factor and mechanism for antigen processing and presentation. Damage and alloreactivity gradients associated with allogeneic HSCT may provide the necessary cellular stress in leukemic blasts to instigate this process. Cell surface expression of the spliceosome complex enables donor-derived antibody production specific to the U5 snRNP200 complex, resulting in leukemia cell injury characterized by cytoskeleton disruption and pore formation and subsequent extravasation of intracellular contents and ultimate leukemia cell demise (oncosis). (B) Emerging immune-directed therapy targeting AML. CAR T cells⁹  as well as other alternative forms of T-cell therapies¹⁰  could be engineered and/or expanded ex vivo to target preferential antigen expression on AML blasts like the U5 snRNP200 complex. NK cells used in the setting of killer cell immunoglobulin-like receptor mismatch allogeneic HSCT can be expanded and potentially engineered to target AML-specific receptors. Monoclonal antibodies, including gemtuzumab ozogamicin (anti-CD33), target AML blasts, and vaccination strategies incorporating AML-specific antibodies could also be considered. Ab, antibody.