In addition to the morphologic similarities, our studies on CCF of WT mice substantiated previous findings in rat hepatocarcinogenesis models and human HCC, particulary increased cell proliferation and metabolic alterations like upregulated glycolysis and lipogenesis and activated Ras/raf-1/MAPK and AKT/mTOR protooncogenic signaling pathways, including an overexpression of the transcription factor chREBP [23, 25]. The gene discussed is RAF1; the disease is hepatocellular carcinoma.