Knockdown of NUP160inhibits cell proliferation, induces apoptosis, promotes autophagyand cell migration, and alters the expression and localization ofpodocyte-related molecules in mouse podocytes. In patients with chronic myeloid leukemia (CML), the expressionof NUP160 is significantly elevated in peripheral blood or cell lines,decreasing the sensitivity of CML to imatinib. Conversely, in human angiosarcoma, the gene fusion NUP160-SLC43A3causes truncation of NUP160, thereby enhancing cell proliferation. The gene discussed is NUP160; the disease is angiosarcoma.