Glucocorticoids, such as cortisol in humans and corticosterone in rodents, are biosynthesized in the intermediate cellular zone of the adrenal cortex, termed as zona fasciculata, and released into peripheral blood under the control of the neuroendocrine hypothalamic-pituitary-adrenal (HPA) axis and the circadian system (Nicolaides, Charmandari, Kino, & Chrousos, 2017; Nicolaides, Kino, Roberts, et al., 2017). Glucocorticoids are sine qua non in maintaining our internal balance, or homeostasis, by influencing a large number of biologic functions, including arousal, cognition, memory, cardiovascular tone, as well as intermediary metabolism, and the immune and inflammatory reaction (Nicolaides, Kyratzi, Lamprokostopoulou, Chrousos, & Charmandari, 2015). At the cellular level, glucocorticoids influence the proliferation rate and differentiation fate of several cells, as well as the programmed cell death (apoptosis). Furthermore, increasing evidence indicates that these hormones cause transient and/or long-term alterations in the epigenome through changes of the methylation of several dinucleotides of cytosine-guanine (CpG) found in the noncoding regions of many genes (Zannas & Chrousos, 2017). The above-mentioned pleiotropic glucocorticoid actions are mediated by an almost ubiquitously expressed protein receptor, the glucocorticoid receptor (GR), which is a member of the group of steroid receptors, which belong to the nuclear receptor family of transcription factors, and induces or represses the expression of a large number of glucocorticoid target genes (Chrousos & Kino, 2005; Nicolaides, Galata, Kino, Chrousos, & Charmandari, 2010).