The results showed that CCC DNA formation was suppressed by two ATR inhibitors (AZD6738 and VE-821) (Fig. 2B and C) and the CHK1 inhibitor (CHIR-124) (Fig. 2B and C), suggesting that the ATR-CHK1 pathway indeed played a critical role in HBV CCC DNA formation during de novo infection. The gene discussed is CHEK1; the disease is infection.