We previously showed that cyclin D1 expression in MM cells activates the UPR pathway and favors cell death through the protein kinase R-like endoplasmic reticulum kinase (or PERK)/activating transcription factor 4 (or ATF4)/CCAAT enhancer binding homologous protein (or CHOP) axis [7]. This evidence concerns the gene CCND1 and Miyoshi myopathy.