In the presence of insulin resistance, the demand for a compensatory increase in insulin secretion from β-cells with a genetically determined high rate of apoptosis early in the physical history of T1D, in addition to cellular stress, would further increase the expression of these insulin/proinsulin molecules and antigen presentation to the immune system, and hence may trigger autoimmunity, inflammation, and β-cell destruction and death (246, 247). The gene discussed is INS; the disease is Insulin resistance.