Insulin resistance which precede the development of T2DM results in a rapid surge in insulin demand, thus triggering the pancreatic β-cells to adapt to this new demand by increasing the mass and function of the β-cell to release sufficient insulin, thus maintaining normal glycemia This compensatory mechanism results in hyperinsulinemia, thus initiating the development of metabolic disorders (Zhang et al., 2019; Rachdaoui, 2020). This evidence concerns the gene INS and type 2 diabetes mellitus.