Two of these compounds, namely AS-06 and AS-29, induced the accumulation of ubiquitinated proteins in human MM cells, suppressing the degradation of IKB-α and the nuclear translocation of p65 in MM cells; they also triggered apoptosis through caspase-8 and caspase-9 activation and cytochrome c release from mitochondria, while decreasing the caspase inhibitors c-IAP-1 and XIAP. Here, XIAP is linked to Miyoshi myopathy.