We hypothesize fromthese observations that DDIT3-mediated induction of reactive oxygen species (87) might exacerbate the replication stress inthe host, which are necessary for the conversion of its rcDNA to cccDNA, furthersuggested by the rescue of HBV-induced replication stress in the absence of DDIT3.As a final consequence of this action, it is likely that DDIT3 overproduction causescell death and inflammation, which can stimulate tumor formation whendysregulated. The gene discussed is DDIT3; the disease is neoplasm.