This effect might be attributed to a decreased inhibitory effect over the local production of IL-1β by interacting with local macrophages [70], which the presence of continued hyperglycemia, elevated free fatty acids, and amyloid deposition [79] leads to continued islet inflammation, β-cell apoptosis, and consequent decreased insulin secretion, observed late in the evolution of T2DM [18]. The gene discussed is INS; the disease is type 2 diabetes mellitus.