Using mouse models, they observed that the transfer of SLAMF6/CD352+ Eμ-TCL1 CLL cells into SLAMF6/CD352−/− recipients, in contrast to wild-type (WT) recipients, significantly induced the expansion of a PD-1+ subpopulation among CD3+CD44+CD8+ T cells, which had impaired cytotoxic functions. The gene discussed is CD8A; the disease is B-cell chronic lymphocytic leukemia.