INS and type 2 diabetes mellitus: Furthermore, emerging evidence reveals that mitochondrial dysfunction underlies insulin resistance and β‐cell dysfunction in T2DM.7 Increased production of mitochondrial reactive oxygen species (ROS) results in the activation of the JNK pathway, which promotes the phosphorylation of serine residues of insulin receptor substrate (IRS1) proteins, instead of tyrosine residues, thereby impairing insulin signalling cascade.