For example, dasatinib, a known ABL inhibitor, was approved to treat ALL with the BCR-ABL1 fusion or fusions involving other ABL class kinases9–11; however, a recent study showed that dasatinib is also effective in T-cell acute lymphoblastic leukemia (T-ALL) that has no ABL alterations and the network-based systems pharmacology analysis identified that LCK is the hidden driver of unexpected dasatinib sensitivity in T-ALL in a non-genetic-dependent manner12. Here, ABL1 is linked to acute lymphoblastic leukemia.