Thus, it is tempting to speculate that nuclear GLS2 participates in the growth-arrest program preventing unlimited cell proliferation, which may explain why certain tumors (e.g. gliomas, hepatomas and lung cancers) showed the opposite behavior: silencing of GLS2 and upregulation of GLS isoforms to keep active their proliferative program3. Here, GLS is linked to hepatocellular carcinoma.