Replacing the original E1A promoter with a tumor-specific promoter can transcriptionally control viral replication to some extent.16 The vital gene for late viral RNA export is E1B 55K, and viruses with an E1B 55K deletion are incapable of replication in normal cells; however, tumor cells can efficiently export late viral RNA in the absence of E1B 55K.17 As a binding partner of adenovirus type 5, the coxsackie and adenovirus receptor (CAR), when expressed on tumor cells, restricts the infection efficiency of adenovirus type 5. This evidence concerns the gene DHTKD1 and neoplasm.