Although we used JAK2-V617F Ba/F3 cells to predict the ruxolitinib resistant mutations, one must focus on other JAK2 variants such as point mutations in JAK2 other than V617F (exon 12 mutations) (9), additional JAK2 point mutations in pediatric or adult B-ALL (54, 55), or active form of JAK2 including TEL::JAK2 (14), PCM::JAK2 (56) and BCR::JAK2 (57) to predict resistance mechanisms against the JAK inhibitors. The gene discussed is BCR; the disease is precursor B-cell acute lymphoblastic leukemia.