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]. This evidence concerns the gene CD68 and acute myeloid leukemia.