Lund University researchers uncovered that acute myeloid leukemia (AML) cells express SLAMF6, an immune checkpoint protein enabling escape from T cell-mediated destruction. By engineering an antibody to block SLAMF6, they reactivated T cells in vitro and humanized murine models, overcoming AML’s immunotherapy resistance. This discovery presents a novel target for AML treatment, advancing therapeutic avenues for this challenging hematologic malignancy.