Although no data has been presented to support this to date, it’s possible that the use of these agents may potentiate the attachment of CTCs to secondary sites that express E-cadherin, such as the liver, lungs and intestines, or may promote mesenchymal-to-epithelial transition (MET) of pre-existing micro-metastases resulting in E-cadherin re-expression, cellular proliferation and subsequent formation of clinically detectable metastases, as has been observed in breast cancer (Chao et al., 2010; Padmanaban et al., 2019). The gene discussed is CDH1; the disease is breast carcinoma.