Emerging lines of evidence indicate that aberrant activation of several signaling cascades, including the activator of transcription (Jak/STAT), epidermal growth factor receptor (EGFR), Ras/extracellular signal-regulated kinase (ERK), CDKN1C/P57, phosphoinositol 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) [3], Cyclooxygenase-2/Snail/E-cadherin, NF-κB [4–7] and HGF/cMET pathways [8, 9] contributes to the pathogenesis of HCC. This evidence concerns the gene CDKN1C and hepatocellular carcinoma.