Thus, in the HepG2-NTCP cells, in the absence of HBV infection or replication, we observed constitutive nuclear pCHK1 staining, which could be blocked, as expected, by inhibitors of the ATR-CHK1 pathway (see Fig. S1A in the supplemental material) but did not appear to be further stimulated by HBV infection under our infection conditions (data not shown). This evidence concerns the gene ATR and infection.