We previously reported that macrolide antibiotics, including clarithromycin (CAM), have an inhibitory effect on autophagy flux and simultaneous inhibition of two major intracellular degradation systems, the ubiquitin-proteasome inhibition by BTZ and the autophagy-lysosome inhibition by CAM systems, which remarkably enhances ER stress-mediated apoptosis along with upregulation of CHOP/GADD153 in MM cell lines and breast cancer cell lines in vitro [18, 19]. The gene discussed is DDIT3; the disease is breast cancer.