In addition, Du Cheng et al. reported that HCV promotes fibrosis through the tumor necrosis factor alpha (TNF-α) and reactive oxygen species (ROS) -MAPK pathways, consistently activating NF-κB, inducing the secretion of chitinase 3-like protein 1 protein (YKL-40), and promoting the progression of HF through the interaction between HCV and YKL-40, suggesting that the upregulation of YKL-40 may improve the success rate of HF modeling [42]. This evidence concerns the gene CHI3L1 and hydrops fetalis.