A possible explanation of our findings is that during proteasome inhibition in MM cells, misfolded proteins are still extracted from the ER, as has been reported for 3-Hydroxy-3-methylglutaryl-coenzyme A reductase in the cholesterol biosynthesis pathway (Morris et al., 2014), and that their removal from the ER alleviates the proteotoxic load. The gene discussed is HMGCR; the disease is Miyoshi myopathy.