In detail, majority of the newer human serotype 5 oAd constructs, like ONCOS-102, LoAd703, TILT-123, ORCA-010, CG0070, under active clinical development contain intact E1B 55 kDa gene to circumvent the attenuation in viral replication capacity, and rather employ different genetic engineering strategies like cancer-specific promoter driven Ad E1A expression or deletion of the Rb binding site in Ad E1A gene to achieve preferential replication in cancer cells (33–38). Here, RB1 is linked to cancer.