MAP3K5 or ASK1 was shown to induce c-Jun N-terminal kinase 1 (JNK/MAPK8/SAPK1) phosphorylation, leading to Bcl-2 activation of cell autophagy, and was associated with endoplasmic reticulum stress, making it a promising therapeutic target for IBD [20]. Here, BCL2 is linked to inflammatory bowel disease.