and significantly suppresses tumor growth in a U266B1 multiple myeloma xenograft model. These findings reframe cytoprotective autophagy not as a resistance liability to be inhibited, but as an inducible degradation capacity that can be redirected to eliminate oncogenic survival factors, suggesting a generalizable strategy for amplifying lysosomal targeted protein degradation through controlled proteostasis stress.
Elshazly et al. (Mon,) studied this question.