Studies have confirmed that the reduction in islet β cells in patients with type 2 diabetes (T2D) is mainly due to a large amount of amyloid deposition inside and outside the islet cells, and the toxic amylin oligomers increase the frequency of β-cell apoptosis beyond its regeneration frequency, with the replication of β cells being more sensitive to the toxicity of amylin oligomers, as well as preferentially apoptotic, leading to a gradual decrease in the number of β cells [13,14]. This evidence concerns the gene IAPP and type 2 diabetes mellitus.