While YM155 does suppress survivin levels in MM cells at higher concentrations, our data indicate that YM155 additionally triggers the ER stress response and abrogates both IL-6 induced as well as constitutive STAT3 signaling, ultimately converging on the inhibition of Mcl-1 expression, an anti-apoptotic factor that has been proven to be essential for MM cell survival [4, 44]. Here, MCL1 is linked to Miyoshi myopathy.