As it has been reported that the genomic profiling of B-ALL at diagnosis and relapse shows substantial changes in both the number and nature of the detected genetic alterations (59), it is possible to speculate that patients expressing wild-type p53 at diagnosis and lacking additional alterations in checkpoint pathways, remain sensitive to a DNA damaging agent but will not benefit from a checkpoint inhibitor (41). Here, TP53 is linked to acute lymphoblastic leukemia.