Further synthetic chalcones induced apoptosis (dimethoxy- or triethoxyphenyl-based chalcones, nitrophenyl chalcones) or autophagy (trans-chalcone), inhibited signaling pathways (AKT by nitrophenyl chalcones, STAT3/STAT5 by thiopyrimidine-chalcone hybrids and Wnt signaling by trans-chalcone), and enhanced ROS formation (dimethoxyphenyl-based chalcones and trans-chalcone) in HCC models [26,27,28,29,30]. This evidence concerns the gene AKT1 and hepatocellular carcinoma.