In cervical cancer HeLa cells, celastrol induced G2/M cell cycle arrest and caused apoptosis, parapoptosis and autophagy via various pathways, including proteasome, ERS and Hsp90 inhibition; apoptosis and parapoptosis promoted cell death, while autophagy was a cytoprotective mechanism in which endoplasmic reticulum apoptosis was caused by celastrol treatment, resulting in the significant upregulation of ERS markers Bip, PERK and IRE1 and causing cytoplasmic vacuolization that was associated with endoplasmic reticulum expansion rather than autophagy (Wang et al., 2012). This evidence concerns the gene ERN1 and cervical carcinoma.