Evidence has also begun to emerge suggesting that resistance to therapy is more prevalent with tumor-targeted agents (particularly when used as single-agents) compared to DNA-damaging chemotherapeutics, which may be due in part to the ability of cancers to alter/mutate the drug target (as in the case of BCR-ABL) or bypass targeted inhibition by rewiring pathways or shifting dependence to compensatory signaling [18–21]. Here, BCR is linked to neoplasm.