Linc-VLDLR is significantly up-regulated in malignant hepatocytes. Exposure of HCC cells to diverse anticancer agents such as sorafenib, camptothecin, and doxorubicin increases linc-VLDLR expression in cells as well as extracellular vesicles (EV) released from these cells. Incubation with EVs reduces chemotherapy-induced cell death and also increases linc-VLDLR expression in recipient cells. RNAi-mediated knockdown of linc-VLDLR decreases cell viability and abrogates cell-cycle progression. Moreover, knockdown of linc-VLDLR reduces expression of ABCG2 (ATP-binding cassette, subfamily G member 2), whereas overexpression of this protein reduces the effects of linc-VLDLR knockdown on sorafenib-induced cell death (1).