A new coronavirus, 2019-nCoV, has caused significant public health threats since December 2019. ACE2, the receptor for SARS-CoV, has been shown to mediate 2019-nCoV infection. However, liver damage is also observed in many patients, and the mechanism remains unclear. This study used single-cell RNA sequencing to evaluate ACE2 expression in healthy liver tissues from two independent cohorts. The results showed specific ACE2 expression in cholangiocytes, not in hepatocytes or other cell types. This suggests that 2019-nCoV may directly infect cholangiocytes, leading to liver damage, rather than hepatocytes. The study also found that ACE2 expression in cholangiocytes is comparable to that in alveolar type 2 cells, which are major targets of SARS-CoV and 2019-nCoV in the lungs. These findings indicate that liver damage in 2019-nCoV patients may be due to cholangiocyte dysfunction, drug toxicity, or systemic inflammation, rather than direct viral damage to hepatocytes. The study highlights the importance of monitoring liver function in 2019-nCoV patients during treatment and recovery. Single-cell analysis revealed that ACE2 is highly expressed in cholangiocytes, suggesting a potential mechanism for viral infection and bile duct damage. The study also notes that technical limitations may affect the detection of low ACE2 expression in hepatocytes. Overall, the findings suggest that liver damage in 2019-nCoV patients may not be caused by direct viral infection of hepatocytes, but by other factors such as cholangiocyte dysfunction or drug-induced injury. This study provides insights into the mechanisms of liver dysfunction in 2019-nCoV patients and emphasizes the need for careful monitoring of liver health during treatment.A new coronavirus, 2019-nCoV, has caused significant public health threats since December 2019. ACE2, the receptor for SARS-CoV, has been shown to mediate 2019-nCoV infection. However, liver damage is also observed in many patients, and the mechanism remains unclear. This study used single-cell RNA sequencing to evaluate ACE2 expression in healthy liver tissues from two independent cohorts. The results showed specific ACE2 expression in cholangiocytes, not in hepatocytes or other cell types. This suggests that 2019-nCoV may directly infect cholangiocytes, leading to liver damage, rather than hepatocytes. The study also found that ACE2 expression in cholangiocytes is comparable to that in alveolar type 2 cells, which are major targets of SARS-CoV and 2019-nCoV in the lungs. These findings indicate that liver damage in 2019-nCoV patients may be due to cholangiocyte dysfunction, drug toxicity, or systemic inflammation, rather than direct viral damage to hepatocytes. The study highlights the importance of monitoring liver function in 2019-nCoV patients during treatment and recovery. Single-cell analysis revealed that ACE2 is highly expressed in cholangiocytes, suggesting a potential mechanism for viral infection and bile duct damage. The study also notes that technical limitations may affect the detection of low ACE2 expression in hepatocytes. Overall, the findings suggest that liver damage in 2019-nCoV patients may not be caused by direct viral infection of hepatocytes, but by other factors such as cholangiocyte dysfunction or drug-induced injury. This study provides insights into the mechanisms of liver dysfunction in 2019-nCoV patients and emphasizes the need for careful monitoring of liver health during treatment.