Crucially, aligning with the heightened tumor growth, the deletion of ATXN3 dramatically increased the frequency of Ki-67+ proliferative cells (Fig. 5, D and E), indicating that ATXN3 reduced tumor progression by inhibiting Galectin-9 degradation, which consequently enhanced the Galectin-9-induced cancer cell apoptosis. Here, MKI67 is linked to neoplasm.