In RMS, both the HSP70 (heat shock 70 kDa protein) inhibitor MAL3-101 and the p97 (valosin containing protein) ATPase inhibitor CB-5083 trigger robust UPR activation, marked by increased eIF2α phosphorylation, ATF4 and CHOP upregulation, and XBP1 splicing, thereby promoting tumor cell death [142]. The gene discussed is XBP1; the disease is neoplasm.