In this case, even though we cannot fully conclude that the blockade of tumor growth of PIWIL1-overexpressing HCC by etomoxir was full because of its inhibition on FAO, the observation that the completed blockade of FAO in PIWIL1-overexpressing HCC using etomoxir lead to a tumor with the same degree with that of wild type HCC indicated that blunting FAO can antagonize the tumor-promoting activity of PIWIL1. The gene discussed is PIWIL1; the disease is neoplasm.