Apoptosis was induced by the upregulation of PUMA and NOXA and their interaction with Bax; carfilzomib can induce autophagy, but this process ends as apoptosis progresses.[165, 166] When combined with chloroquine, the autophagic process of carfilzomib results in enhanced apoptosis in vitro and in vivo, increased CRT exposure via danger signals from apoptotic cells, induction of ICD in myeloma cells, and stimulation of the immune response to myeloma. The gene discussed is CALR; the disease is plasma cell myeloma.