To delineate the molecular mechanism behind MYC-mediated transcriptional repression of Type I IFN signaling, we compared levels of STAT1, STAT2 and IFNα2 in MYC-driven lymphoma cell lines overexpressing MYC, or a MYC mutant that fails to sequester MIZ1 (MYC V394D), or the corresponding empty vector (EV). The gene discussed is STAT1; the disease is lymphoma.