Acute myeloid leukemia (AML) exhibits extensive metabolic reprogramming, by which the cancer cells utilize glucose for their leukemic proliferation and survival. Monocytic leukemia THP-1 cell line is used as the a standard model for investigating these glucose-dependent metabolic and epigenetic landscapes. These regulation landscapes is essential for translating metabolic insights into clinical AML pathogenesis. I aim to recruit in-house NGS cell line data with large public NGS datasets and to integrate multiple NGS data, including but not limited to mRNA-Seq, totalRNA-Seq, smallRNA-Seq and the art-of-state RADICL-Seq, to elucidate the change of epigenetic regulation associated with glucose change in AML cells.