Liver cancer is among the most common types of cancer worldwide. Between 2007 and 2017, liver cancer ranked 7th on the list of cancers with the highest global incidence. Through carcinogenesis, cancer cells go through complex and dynamic phenotypical changes -epithelial-to-mesenchymal transition (EMT), or its reverse mesenchymal-to-epithelial transition (MET)- to cope with metastasis rate-limiting steps. Tumor cells gain metastatic properties in EMT, whereas cells acquire tumor forming capabilities in MET. Growing evidence suggests that cells showing both types of properties are most likely to contribute metastatic outgrowth and resistant to therapeutics. Now, a new study has identified a pivotal molecular mechanism that gives rise to this “hybrid epithelial/mesenchymal (E/M)” state. Experiments on human liver cancer cells indicated that the process modulated by lncRNA HOTAIR, a non-coding RNA that contributes to metastasis and poor prognosis in liver cancer. In tumor cells, lncRNA HOTAIR over-expression suppressed the expression of c-Met which is a promising target for liver cancer treatment and therapy resistance. c-Met suppression by lncRNA HOTAIR repressed individual cell scattering but enhanced metastatic ability by promoting cooperative migration and survival in circulation. Understanding how this fatal balance is maintained could help researchers and clinicians deliver better care to patients with persistent forms of liver cancer.