Recently, the disruption of chromatin-dependent processes that suppress c-MYC activity—such as the inhibition of the BET bromodomain protein Brd4 by JQ1—has shown promising results in experimental models of multiple myeloma, BL, acute myeloid leukaemia, acute lymphoblastic leukaemia and neuroblastoma68, 69. The gene discussed is MYC; the disease is AL amyloidosis.