Figure 1.

(a) Induction of autophagy in cells with defective GABARAP expression restores Golgi-mediated calreticulin exposure in multiple myeloma. The absence of GABA type a receptor-associated protein (GABARAP) in high-risk multiple myeloma impairs autophagy and interferes with bortezomib-induced immunogenic cell death (ICD) by disrupting calreticulin (CALR) relocation, reducing dendritic cell phagocytosis and limiting anti-tumor T cell responses (A). Rapamycin restores autophagy, facilitates Golgi vesicular transport and reinstates CALR exposure, thus enhancing ICD in GABARAP-deficient cells treated with bortezomib (b). Combining bortezomib with rapamycin may overcome ICD resistance in MM patients with defective GABARAP expression.