In contrast, the CRAd strategy allows these off-target cells to be infected, but aims to prevent the virus from executing its lethal lifecycle in non-cancer cells by controlling early gene E1 or E4 expression with cancer-specific promoters, or by mutating the ability of E1A or E1B proteins to interact with pivotal cellular proteins like pRB, p53, or p300 pathways ([12,24,25,26,27], and reviewed in [7]). This evidence concerns the gene DHTKD1 and cancer.