The maltonis-dependent upregulation of IFN-α and -γ antiviral response and the concomitant decreased cell survival and cell cycle modulation (Supplementary Fig. S3A, B) further confirm this view and is in line with recent observation that inhibition of both EZH2 and G9a histone methyltransferase activities suppresses cell proliferation in multiple myeloma, through the induction of an interferon response [41, 42]. The gene discussed is EHMT2; the disease is AL amyloidosis.