In summary, with a focus on B-ALL due to the greater need for improved therapies compared to CML, which in most patients is well controlled by treatment with tyrosine kinase inhibitors17—these results suggest that microenvironmental ANXA2 deficiency attenuates induction of BCR-ABL1+ B-ALL, possibly due to inhospitality of the BMM. The gene discussed is ANXA2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.