β-Arrestin1 competes with IRS proteins for ubiquitination and degradation, such that β-arrestin1 deficiency accelerates insulin-induced IRS degradation, exacerbating cellular insulin resistance, whereas overexpression of β-arrestin1 restrains this process, leading to increased insulin signaling downstream of IRS-1 and improving cellular insulin sensitivity (122). The gene discussed is INS; the disease is Insulin resistance.