Moreover, the combination of MEK1/2 inhibitors with traditional cytotoxic chemotherapy may counteract resistance to chemotherapy in relapsed ALL, as MEK2 knockdown or inhibition increases sensitivity to chemotherapy in a p53-dependent manner.[3] Although these experiments were performed in vitro, ex vivo, and in vivo in mice, pediatric clinical trials are underway and could expedite the clinical application of these MEK inhibitors in Ph+ ALL. The gene discussed is MAP2K2; the disease is acute lymphoblastic leukemia.