Researchers at Lund University identified a novel immune escape mechanism in acute myeloid leukemia (AML) involving the surface protein SLAMF6, expressed in approximately 60% of AML cases but absent on healthy hematopoietic stem cells. Using CRISPR/Cas9 gene editing, they demonstrated that removing SLAMF6 in AML cell lines reactivated T cells, restoring anti-leukemia immune responses. They engineered an antibody to block SLAMF6, which reinvigorated T cell activity in vitro and in humanized mouse models. This discovery provides a new therapeutic target to overcome immune resistance in AML, an area with limited effective immunotherapies despite major advances recognized by the 2025 Nobel Prize contributions in peripheral immune tolerance.