Lund University researchers have identified the SLAMF6 surface protein as an immune checkpoint mediating acute myeloid leukemia's (AML) evasion from immune attack. SLAMF6, expressed on AML stem cells but absent on healthy hematopoietic stem cells, suppresses T cell activity. Utilizing CRISPR/Cas9 and antibody engineering, the team demonstrated that blocking SLAMF6 restores T cell cytotoxic function against AML both in vitro and in humanized mouse models, thereby representing a promising therapeutic target.