Therefore, if sepsis-induced PPARβ/δ activation is GR-dependent (as suggested by the results in dexamethasone-treated myotubes, see Figure 3C), it may reflect other mechanisms than increased GR abundance, for example an increased interaction between the GR and PPARβ/δ as suggested by results in dexamethasone-treated myotubes (See Figure 3D). The gene discussed is NR3C1; the disease is Sepsis.