The increasing appreciation of the importance of autophagy as consequence of 
cancer therapy or underlying disease biology is illustrated by the large number 
of papers that are evaluating autophagy as a cancer target. While autophagy is 
often linked to the generation of metabolic precursors, it is also important in 
diseases where protein production is a hallmark of the disease itself, such as 
pancreatic cancer and multiple myeloma. Multiple myeloma is characterized by 
ongoing autophagy as a consequence of constitutive immunoglobulin production, 
which creates the need for efficient transfer and disposal of misfolded or 
unfolded proteins. In order to survive this cellular stress, plasma cells depend 
on proteasomal degradation of the large volume of misfolded proteins as well as 
the autophagy pathway. It has previously been suggested that the excess proteins 
not targeted to the proteasome, or that accumulate when the proteasome is 
inhibited through the use of chemically active agents such as bortezomib, are 
linked to impaired cell survival, and that their packaging in the form of an 
aggresome somehow minimizes their 'proteotoxicity' allowing these toxic proteins 
to be sequestered away from normal cellular machinery.