The examples are inhibitors targeting ABL1/ABL2, which increased the response rate among ALL patients with translocation t(9;22) (q34;q11), resulting in breakpoint cluster region–Abelson murine leukemia viral oncogene homolog 1 (BCR–ABL1) gene fusion (Philadelphia chromosome), or inhibitors of Janus kinase 2 (JAK2), which improved treatment outcome of individuals with Philadelphia chromosome-like ALL (Ph-like ALL) [14]. The gene discussed is ABL1; the disease is acute lymphoblastic leukemia.