While HGF signaling through its receptor c-Met has been reported to have a beneficial role in preventing fibrosis and NASH,19,20 HGF/c-met signaling is considered pro-oncogenic for HCC where its inhibition is thus a therapeutic strategy (eg, clinical trial NCT02115373 with c-Met inhibitor Tepotinib). This evidence concerns the gene MET and metabolic dysfunction-associated steatohepatitis.