EMT is widely thought to be one of the most important mechanisms in cancer metastasis 32; thus, we measured levels of E‐cadherin, an epithelial phenotype marker, N‐cadherin and vimentin, markers of the acquired mesenchymal phenotype, and Twist, a nuclear transcription factor, in HJC0152‐treated NSCLC cells.45, 46 Our results demonstrated that HJC0152 treatment interrupted the EMT process during cancer invasion, thus providing a rationale for treating invasive, progressive and metastatic cancers with HJC0152. The gene discussed is VIM; the disease is metastatic malignant neoplasm.