In a study of differentially expressed molecular profiles associated with HBV-mediated HF, the key role of oxidative stress in the progression of HF was revealed, suggesting that catalase (CAT), biliverdin Reductase B (BLVRB), nucleoredoxin (NXN), peroxiredoxin 1 (PRDX1), and isocitrate Dehydrogenase 1 (IDH1) may be potential therapeutic targets for HF [39]. The gene discussed is NXN; the disease is hydrops fetalis.