CLK4 was overexpressed in mesenchymal-like TNBC (MES-TNBC) cells and correlated with poor patient survival.114 Silencing of CLK4 in a xenograft mouse model was shown to decrease the expression of multiple epithelial-mesenchymal transition (EMT) genes which participate in metastasis and repress tumor cell migration in TNBC cells.114 Notably, depletion of CLK4 impaired the expression of SMAD3, a mediator of TGF-β signal transduction, suggesting that overexpression of CLK4 can promote metastatic and aggressive phenotypes in MES-TNBC cells. Here, CLK4 is linked to neoplasm.