The yin and yang of autophagy in AL amyloidosis

In this issue of Blood, Oliva et al report on a series of experiments that have demonstrated that in systemic light chain (AL) plasma cells (PCs), there is a complex interaction between those PCs and the immunoglobulin light chains (LCs) they produce.¹ The pathology introduced by these unstable amyloidogenic LCs occurs not only at distant organs^2,3 but also in the plasma cells that produce them. This manuscript attempts to unravel the relationship of AL LCs and the PCs that produce them in the context of AL PC susceptibility to proteasome inhibitors and the role autophagy may play in that susceptibility.