We previously reported that UBR5 drove 4T1 tumor metastasis primarily in a cell-autonomous manner and CRISPR-mediated deletion of Ubr5 caused the reduction of the expression of several metastasis-promoting molecules including β-catenin and E-cadherin, as well as altering the cell morphology from an epithelial type to a mesenchymal type [5, 6]. Here, UBR5 is linked to neoplasm.