ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive: 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.