However, UPR activation, as revealed by XBP1 and CHOP presence, is weakly induced or inhibited by Hsp90 inhibitors in a time- and dose-dependent manner in MM cells [48]; moreover, treatment of MM cells with two classical ER stress inducers, such as tunicamycin or thapsigargin, failed to modulate MICA or MICB expression, suggesting that UPR activation, per se, is not sufficient to enhance levels of these ligands and that it is not involved in their regulation by drugs targeting Hsp90 [22]. This evidence concerns the gene DDIT3 and Miyoshi myopathy.