Furthermore, the human islet amyloid polypeptide (h-IAPP), also characteristic of T2D, induced dysfunction of autophagy and apoptosis through CHOP, but inhibition of CHOP alone may not be a durable therapeutic strategy for the β-cell toxicity of h-IAPP, considering multiple stress pathways are activated during this process (176). This evidence concerns the gene DDIT3 and type 2 diabetes mellitus.