We also show that expression of FAM167A is highly upregulated in CD34+ CML cells from patients with BCR-ABL-independent TKI resistance (similar to that in CML cell lines), and that FAM167A is responsible for BCR-ABL-independent TKI resistance: neutralizing FAM167A reversed TKI resistance in cultured cells and in a mouse tumor model. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.