In addition to classical EMT markers, such as E-cadherin, β-catenin, and vimentin, many protein kinases have been reported to promote EMT including CDKL2 [28], also known as p56 or KKIAMRE; it belongs to a cdc2-related serine/threonine protein kinase family [29, 30] and was reported to induce EMT, tumor formation, and metastasis by activating a ZEB1/E-cadherin/β-catenin-positive feedback loop in several human breast cell lines and in orthotopic breast cancer xenograft model [17], which supported an oncogenic role of CDKL2 and was consistent with our results. This evidence concerns the gene VIM and breast cancer.