Together, the above data indicate that HBV suppresses NFAT5 expression by inducing hypermethylation of the AP1-binding site in the NFAT5 promoter, in addition inhibiting NFAT5 through miR-30e-5p targeting of the MAP4K4 signaling pathway, and the inhibition of NFAT5 enhances HCC tumorigenesis by promoting the expression of DARS2 as a downstream target gene (Fig. 5h). Here, NFAT5 is linked to hepatocellular carcinoma.