Abnormal splicing of the ketohexokinase (KHK) transcript resulting in the isoform switch from high-activity ketohexokinase-C to low-activity ketohexokinase-A enhances PRPS1-dependent nucleic acid synthesis and inhibits the regulatory role of fructose metabolism regarding the manufacturing of phosphate, ATP, and reactive oxygen species (ROS), thereby driving hepatocellular carcinoma development [14]. This evidence concerns the gene KHK and hepatocellular carcinoma.