As in many cancer types, BCL2 is highly expressed in CML, particularly in the LSC population, and is perhaps activated by PI3K/AKT and JAK/STAT activity downstream of BCR-ABL1, which supports the development of anti-BCL2 agents to deactivate resistant LSCs54. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.