Hyperactive Raf-MEK-ERK signalling is implicated in hepatocellular cancers, and a recent study has reported increased cell death in Sorafenib (Raf inhibitor)-treated hepatoma cells knocked down for ATG7 (ref. 43), suggesting that therapeutic benefit in Sorafenib-treated ATG7-deficient hepatoma cells may have occurred from a more robust inhibition of ERK signalling. This evidence concerns the gene RAF1 and hepatocellular carcinoma.