In HCC, hypoxia or TGF-β stimulation enriches LncROR within tumor-derived exosomes; uptake of these vesicles by naïve HCC cells elevates LncROR levels, attenuates sorafenib- or doxorubicin-induced apoptosis, and expands the CD133+ CSC pool via TWIST1 activation and p53 pathway inhibition [54]. Here, PROM1 is linked to neoplasm.