Both antiproliferative and pro-apoptotic effects were driven by a mechanism involving BRD4 displacement from MYC, FGFR3, IL6R, and NSD2 enhancers, with a concomitant reduction in the corresponding mRNA levels and an increase in myeloma cells sensitivity to JAK inhibitors, thus arising the possibility of obtaining therapeutic advantages from the combination of these two kind of compounds [82]. Here, IL6R is linked to plasma cell myeloma.