The IS defects were significantly more pronounced when the conjugation assays were performed using CD8+ cells from CLL patients and allogeneic CLL cells (Supplementary Fig. 2), suggesting that in vivo CD8+ cell conditioning exacerbates their inability to form the IS, likely through the combination of indirect mechanisms, mediated by CLL-derived soluble factors, and direct interactions involving multiple surface receptor-ligand inhibitory pairs [12]. This evidence concerns the gene CD8A and B-cell chronic lymphocytic leukemia.