Researchers at Lund University identified SLAMF6, a surface protein expressed on approximately 60% of acute myeloid leukemia (AML) cases, which acts as an immune-suppressive shield enabling leukemia cells to evade T cell-mediated killing. Using an engineered antibody to block SLAMF6, T cell activity was restored in vitro and in humanized mouse models, reactivating anti-leukemia immunity. This finding reveals a novel immune escape mechanism and potential therapeutic target to overcome treatment resistance in AML.