The expression of eEF2K has been reported to be causally associated with tumor cell invasion and metastasis[3, 15] and mediates epithelial‐to‐mesenchymal transition (EMT).[18] We showed that C1 treatment remarkably inhibited the cell migration and invasion of TNBC cells in wound healing and transwell assays (Figure5A,B) and led to an increase in the expression of E‐cadherin and a decrease in the expression of N‐cadherin and Vimentin (Figure 5C). Here, EEF2K is linked to neoplasm.