To identify the downstream effectors of FLT3 in drug resistant CML cells, we performed RNA-seq analysis of FLT3-dependent TKI-resistant K562-FLT3-IR (imatinib-resistant), K562-FLT3-NR (nilotinib-resistant), and FLT3-independent K562-IMR (spontaneous imatinib-resistant), K562-NLR (spontaneous nilotinib-resistant) [15] cells and examined key oncogenes and signaling pathways frequently altered in cancers. The gene discussed is FLT3; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.