DHTKD1 and neoplasm: Previously, diverse schemes have been developed to engineer specificity and improve safety of virotherapy strategies with oncolytic adenovirus, among which are involvement of the E1B deletion [31] or E1A mutation [32], introduction of tumor- or tissue-specific promoters to control the expression of E1A or/and E1B [33]–[35], utilizing liver-specific miR-122a to regulate E1A expression [27], and genetic modification of the adenoviral capsid to change the adenovirus tropism [36]–[38].