Results: The morning urine copper/zinc ratio and 24hr urinary copper excretion correlated well (r=0.758, P < 0.001). The median of morning urine copper/zinc ratio, 24hr urine copper/zinc ratio, 24h copper excretion, and 24h zinc urinary excretion were 0.370, 0.394, 87.1 and 398.7 in WD group, and 0.051, 0.061, 24.2 and 358.9 in the non-WD group respectively. The differences of morning urine copper/zinc ratio, 24hr urine copper/zinc ratio, and 24h copper excretion were significant (Z-value -6.502, -6.020 and -6.208 respectively, all P values < 0.000 CHD1L is a recently discovered oncogene localized at 1q21, one of the most frequently amplified chromosomal regions in HCC. Herein, by yeast-two hybrid assay, we demonstrate that the anti-apoptotic ability of CHD1L is associated with its interaction with Nur77, a critical member of a p53-independent apoptotic pathway. As the first cellular protein identified to bind Nur77, CHD1L inhibits the nucleus-to-mitochondria translocation of Nur77, and subsequently hinders the release of cytochrome c and the initiation of apoptosis ( Figure 1 ). Further study found that C-terminal Macro domain of CHD1L is responsible for the interaction with Nur77, and a CHD1L mutant lacking residues 600-897 failed to interact with Nur77 and prevent Nur77-mediated apoptosis. We also find that CHD1L confers cellular chemoresistance to drugs that induce apoptosis via the Nur77-mediated pathway, which may lead to the identification of new therapeutic targets for HCC treatment.