In most investigations, reduced levels of RASSF1A were found to be ubiquitous in HCC regardless of the etiologic factors associated with tumor development (hepatitis B or C chronic infection, alcohol consumption, exposure to food contaminated by aflatoxin B1, etc.), strongly suggesting that universal inactivation of RASSF1A in liver cancer is required for hepatocarcinogenesis [6, 16–22]. Here, RASSF1 is linked to liver cancer.