Since (i) HBx activity is promoted in CLD by oxidative stress [64], (ii) integration and intrahepatic accumulation of HBx directly correlate with the progression of CLD [114,115], and (iii) HBx constitutively activates pro-inflammatory molecules, such as NF-κB [67,68], it can be inferred that amelioration of CLD will also attenuate HBx expression and activity, thereby contributing to a functional cure. This evidence concerns the gene NFKB1 and congenital secretory chloride diarrhea 1.