Since increase of the cccDNA pool occurring via intracellular cccDNA amplification should have led to a detectable increase of total intrahepatic cccDNA amounts even in the absence of new infection events, we concluded that cccDNA amplification within already infected human hepatocytes barely took place in humanized mice in the absence of NTCP-mediated entry of new virions. This evidence concerns the gene SLC10A1 and infection.