Although activating mutations in HRAS are observed considerably less frequently in liver cancer compared to NRAS or KRAS [4, 9, 14], our data show that activated HRAS has an oncogenic potential equal to that of NRAS or KRAS counterparts in the liver, calling for further research to explain the biased mutation frequencies among the RAS isoforms found in human cancers. The gene discussed is KRAS; the disease is cancer.