However, in hepatic insulin resistance, gluconeogenesis is increased likely because of increased GR inhibitory proteins that block the negative feedback loop of glucocorticoids [33], such as the non-glucocorticoid binding isoform [34], GRβ [35], and others that bind to the GR steroid receptor complex, such as FKBP51 [36]. The gene discussed is FKBP4; the disease is Insulin resistance.