Philadelphia (Ph)-like acute lymphoblastic leukemia (ALL) is a molecular subtype of high-risk B-cell ALL characterized by formation of abnormal gene fusions involving tyrosine kinase (TK) and cytokine receptor genes and activation of TK signaling.
In this issue of Cancer Cell, Roberts et al. describe the identification of genetic alterations that lead to activated kinase and cytokine receptor signaling in Ph-like ALL and demonstrate that this aberrant signaling can be inhibited effectively.