Off-target effects of carfilzomib that cause cardiotoxicity

In this issue of Blood, Efentakis et al report using an animal model to study carfilzomib (Cfz)-induced cardiotoxicity and to demonstrate that the molecular mechanism is not related to the inhibition of the proteasome function but instead has an influence on modulation of the autophagy pathway, inactivation of AMPKa, and upregulation of PP2A phosphatase activity.(1)