The different phenotypes could be speculated to arise from 1) the complexity of erythrocyte differentiation in vivo, which involves the coordination of a network of transcription factors and epigenetic regulators from surrounding cells; 2) the possibility that other pathways in vivo may compensate for Mgat3-KO–mediated deficiencies; and 3) the role of BCR-ABL, formed by a reciprocal chromosomal translocation to create an aberrant BCR-ABL gene on chromosome 22, which is critical to the pathogenesis of CML due to its effects on aberrant cell signaling. This evidence concerns the gene MGAT3 and chronic myelogenous leukemia, BCR-ABL1 positive.