We developed several types of survivin-responsive m-CRAs (Surv.m-CRAs) in which adenoviral E1A was regulated by the promoter of survivin; in some versions of these viruses, the p53-binding domain in E1B was deleted (i.e., E1B55KD), the Rb-binding domain in E1A was deleted, or the native E1B promoter was replaced with another cancer-specific promoter [11,12]. This evidence concerns the gene DHTKD1 and cancer.