According to this study, the effect was mediated by the endoplasmic reticulum stress response and mitochondrial dysfunction [48] Finally, in a recent report, Lin et al. [49] showed that protodioscin could be responsible for endoplasmic reticulum stress-dependent apoptosis in human cervical cancer cells, likely through the stimulation of the JNK and p38 pathways. Here, MAPK8 is linked to cervical carcinoma.