In fact, in patients with obesity and prediabetes, beta cells are genetically susceptible to functional and oxidative damage associated with insulin resistance and, after years of metabolic stress due to increased insulin production, show a progressive reduction, up to functional exhaustion, through three main mechanisms, including functional metabolic alterations, cell death, and loss of differentiation, an effect considered to be the most relevant to date. The gene discussed is INS; the disease is Insulin resistance.