To explore the clinical relevance of these results in humans, we subsequently investigated the expression of PD-1 in primary and xenografted human B-ALL samples, including those of the PAX5-alt subtype (where CD19 expression is maintained because the activation of the CD19 promoter in human B-ALL cells is not solely dependent on PAX5 activity [52]) and ETV6::RUNX1+ and hyperdiploid subtypes. This evidence concerns the gene PDCD1 and acute lymphoblastic leukemia.