INS and diabetes mellitus: IRE1α becomes active when phosphorylated in response to ER stress [45] and in turn activates c-Jun terminal kinase (JNK) and IκB kinase, both of which impair insulin signaling by phosphorylating IRS1 on serine residues.[46] PERK, which is activated by saturated acids and lipopolysaccharides, inhibits insulin signaling by directly phosphorylating IRS1 or activating JNK.[47] Nothing is known about the role of PDIA4 in cell growth and viability in pancreatic β-cells, or about its role in diabetes.