Many studies have shown that tunicamycin (TM), a naturally occurring antibiotic, can inhibit N-linked glycosylation in several types of cancer cells, presenting a useful therapeutic approach for cancer therapy by decreasing angiogenesis [4], inducing endoplasmic reticulum stress-induced autophagy and apoptosis, and increasing TRAIL-induced cell death (apoptosis) [5,6,7]. The gene discussed is TNFSF10; the disease is cancer.