In contrast, high expression of HMOX1 was observed in liver of LEC rats at the stage of hepatoma [23] suggesting that Cu exposure times and/or inflammation signals might play an additional role for HMOX1 gene induction observed in vivo. Notably, ceruloplasmin synthesis, that is impaired after ATP7B malfunction [8], links Cu to iron homeostasis indicating that lower HMOX1 expression could be related to altered heme, a potent inducer of HMOX1. However, understanding the molecular events between ATP7B impairment and HMOX1 expression needs further work. This evidence concerns the gene CP and hepatocellular carcinoma.