For example, LINP1 is highly expressed in patients with acute myeloid leukemia (AML), but down-regulated in patients with complete remission after treatment; LINP1 enhances HNF4a-AMPK/WNT5A signaling pathway activation and promotes AML progression, and knockdown of LINP1 significantly inhibits AML cells of glucose absorption and survival. The gene discussed is WNT5A; the disease is acute myeloid leukemia.