Other research discovered that ATL I causes overexpression of CD14 or CD14/CD68, improves phagocytosis, and induces death and differentiation in human K562 chronic myeloid leukemia (CML), Jurkat T lymphoma cells, and U937 acute myeloid leukemia (AML), which has the potential to develop new leukemia treatments [57]. Here, CD68 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.