Exposure to BTZ results in TLR4 activation (upregulation) in MM cells [4], leading to protection against BTZ-induced ER stress and ultimately favoring an anti-apoptotic effect through suppression of PERK/ATF4/CHOP branch [12], which are all part of a complex process known as UPR. This evidence concerns the gene EIF2AK3 and Miyoshi myopathy.