The significant increase in the number of PCNA+ β-cells in the diabetic group indicates that either the β-cells are attempting to replicate as a compensatory response to peripheral insulin resistance and/or that the increase in PCNA expression is a DNA repair response to overcome the effects of pro-apoptotic stimuli including elevated circulating levels of glucose and free fatty acids - a consistent pathological feature of type 2 diabetes [51], [52], [53]. Here, PCNA is linked to type 2 diabetes mellitus.