Although these molecular alterations may occur, evidence suggests that defects in proximal insulin signalling, including compromised insulin receptor function or alterations in the expression or number of receptors, are not the major factor contributing to insulin resistance in T2D, especially as insulin-binding studies have demonstrated that a small fraction (2.4%) of total insulin receptors is sufficient to elicit maximal signalling, supporting the term “spare receptor” hypothesis [215,216]. The gene discussed is INS; the disease is Insulin resistance.