Next, we investigated the hetero-gapmer DOCK11-induced suppression of HBV replication and HBV cccDNA levels in the AAV8-HBV1.3mer infection model, which was generated by infecting wild-type C57BL/6J mice using 1 × 1010 copies/mouse of AAV8-HBV1.3mer viral particles leading to the peak of HBV replication approximately 30 days after infection.19 This evidence concerns the gene DOCK11 and infection.