A metabolic switch in proteasome inhibitor resistant multiple myeloma ensures higher mitochondrial metabolism, protein folding and sphingomyelin synthesis

Proteasome inhibitors (PI) have evolved as the central backbone of treatment for multiple myeloma (MM), with first-in-class bortezomib and second-and third-generation PI, carfilzomib and ixazomib, having been approved for this indication.[1][1] Proteasome inhibition disrupts the unfolded protein