In a third study, Matsubara et al. [36] investigated two isoforms of GR in both patients with MDD and with BPD: GRα, which is able to directly exert glucocorticoid effects, and GRβ, which binds poorly to glucocorticoids and, by forming heterodimers with GRα, impairs ligand binding of this isoform and acts as a dominant negative regulator of GR function [36]. This evidence concerns the gene NR3C1 and major depressive disorder.