NOS3 and endothelial dysfunction: While both bortezomib and carfilzomib could theoretically produce endothelial dysfunction through proteasome inhibition–mediated eNOS modulation, the irreversible proteasome inhibition and higher potency of carfilzomib [7] and, perhaps more importantly, the dose-limiting neuropathy associated with bortezomib treatment could potentially explain why the sequelae of endothelial dysfunction may not be observed as frequently with bortezomib treatment.