The disruption of SETDB1 in AML cell lines triggers a type-I IFN antiviral response by desilencing both the LTR and non-LTR elements, indicating that the evasion of innate immune sensing of EREs possibly underlies the poor prognostic impact of SETDB1 alterations in AML and MDS (51). The gene discussed is SETDB1; the disease is acute myeloid leukemia.